Review Report

Selenium in cattle diseases and reproductive health

Carol Majors,‡ Andrew Myers,† Ramanathan Kasimanickam

College of Veterinary Medicine, Washington State University, Pullman, WA, USA

Abstract

Selenium (Se) is a trace mineral critical for antioxidant activity, immune function, thyroid hormone conversion, fetal development, and reproduction. The goal is to emphasize the importance of preventing Se deficiency in cattle through year-round supplementation, soil analysis, and appropriate treatments to avoid conditions like white muscle disease, nutritional muscular dystrophy, and reproductive issues. Certain US regions have Se-deficient soils that may produce Se-deficient forages. In these areas, Se deficiency-related syndromes are common. Cattle require 0.1 mg/kg of Se for maintenance and more during pregnancy or lactation. Across age groups, deficiency results in various clinical manifestations, including white muscle disease in neonates, nutritional muscular dystrophy in calves and yearlings, and reproductive dysfunction in adults. Diagnosis involves soil and pasture analyses, Se concentrations in blood and serum, erythrocyte glutathione peroxidase activity, liver biopsies, or tissue recovery at slaughter or necropsy. Treatment is generally ineffective for neonates, but can be successful in older cattle, with injectable Se and ongoing supplementation being key. Prevention through year-round supplementation is crucial in Se-deficient regions.

Keywords: Nutrition, selenium, food animal, health, reproduction

 

Citation: Clinical Theriogenology 2025, 17, 12015, http://dx.doi.org/10.58292/CT.v17.12015

Copyright: © 2025 The Author(s). This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/), permitting all noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Published: 04 August 2025

‡Current address: Soda Springs Animal Clinic, Soda Springs, ID, USA

†Current address: Verona Veterinary Medical Service, Verona, WI, USA

Competing interests and funding: None to declare.

CONTACT: Ramanathan Kasimanickam ramkasi@wsu.edu

 

Introduction

Selenium (Se) is a trace element with important roles in animal health and performance. In cattle, Se deficiency can have economically important impacts such as reduced fertility, retained fetal membranes (RFM) and increased mastitis and metritis.1 This review includes the importance of meeting Se requirements for cattle, how to recognize clinical manifestations across age groups, and using year-round Se supplementation to prevent deficiency-related conditions, such as enzootic (nutritional) muscular dystrophy (NMD) and reproductive dysfunction in adult cattle.2,3

Selenium is a naturally occurring trace mineral with a critical role in bovine health; however, its availability in soil and forage varies widely across the US. Areas with Se-deficient soils (e.g. the Pacific Northwest) are at particularly high risk for Se deficiency in cattle, leading to a range of issues, from neonatal diseases to reproductive and metabolic problems in adults.4 Understanding the role of Se in cattle, clinical signs of deficiency, and methods for diagnosis, prevention, and treatment, are essential for effective herd management.

There is considerable variation in soil Se concentrations across the continental US (Figure 1),5 with markedly lower soil Se concentrations in the Northwest, Northeast, Southeast, and Great Lakes states. Soils with concentrations < 0.05 ppm are considered critically low, whereas concentrations above this threshold are generally considered adequate. However, Se deficiency does not depend solely on soil Se concentrations, as deficiency in cattle occurs because of Se absorbed by plants that is influenced by soil pH and availability of Se compounds in soil.

Figure 1.
Figure 1. Color-coded map of relative Se concentrations in soil samples for counties in the continental US. Soil Se < 0.05 ppm is critically low; higher values are considered adequate, depending on soil pH and Se availability to plants4-9

Critically low soil Se concentrations lead to forages with < 0.1 ppm Se in > 80% of cases, often resulting in deficiencies in unsupplemented cattle. In areas with variable soil Se concentrations (Figure 2),6 forages are roughly split between deficient and adequate; therefore, some cattle may still develop Se deficiencies despite adequate soil concentrations.

Figure 2.
Figure 2. Distribution of forages generally deficient, relatively low, and adequate in Se6

As forages obtain their Se from soil, the distribution of Se-deficient areas in cattle generally mirrors the distribution of soil Se concentrations, albeit not perfectly. Selenium-deficient soils substantially increase the risk, but do not guarantee Se-deficient cattle.

Selenium deficiency in south Atlantic seaboard’s soil is largely attributed to costal deposits washed from highly weathered land masses. The northeastern states’ soil predates cretaceous period selenization; seleniferous cretaceous shales did not weather in these areas, resulting in low soil Se concentrations. Much of these cretaceous sedimentary shale rocks weathered into the central and northcentral states from Montana and North Dakota, through Wyoming, Colorado, and South Dakota, resulting in soils that produce forages with variable or adequate Se.7

Washington state is riddled with volcanoes; 5 are active and have erupted relatively recently, with volcanic deposits creating very low soil Se concentrations.7 Current agricultural practices (e.g. intensive cropping) can further decrease soil Se concentrations.

Selenium requirements

Daily Se requirements for cattle are 100 μg/kg dry matter (DM) for beef cattle, 300 μg/kg DM for dairy cows and 100 μg/kg DM for calves.1 There is a close link between Se and vitamin E status, as well as antioxidant status.8 Vitamin E has a key role in Se absorption and utilization.9 Selenium and vitamin E have interdependent antioxidant functions; therefore, low vitamin E intake may increase the Se required to prevent some conditions.9

The National Academies of Sciences, Engineering, and Medicine (NASEM; formerly National Research Council, the operating arm of the NASEM) recommends a daily intake of 15-60 IU of vitamin E for adult cattle, whereas nursing calves require 40-60 IU.10,11 Deficiencies in either Se or vitamin E can impair thyroid metabolism, decrease growth rate, reduce fertility, alter phagocytic response, and lower disease resistance.12

Certain dietary components can negatively impact Se absorption in cattle. Diets rich in carbohydrates, nitrates, sulfates, calcium, or hydrogen cyanide (e.g. from clover forage or flax seeds) can interfere with Se utilization. Sulfur competes with Se for absorption at concentrations > 2.4 g/kg DM. Similarly, ferric iron can reduce Se absorption by forming insoluble complexes that are not assimilated by enterocytes.13

Calcium also influences Se absorption; concentration of 0.8% DM in the feed supports optimal Se absorption in dairy cows during late pregnancy.14 However, calcium supplementation in beef cattle, especially at concentrations typically used in intensive production, significantly reduces muscle Se concentrations.15 Additionally, high concentrations of lead in a calf diet can decrease both serum and tissue Se concentrations.16 It should also be noted that any lead exposure sufficient to affect Se concentrations is likely to present a food safety risk. The primary concern for the practitioner should be the adulterated meat from these animals, rather than Se deficiency.

Iodine deficiency can exacerbate Se deficiency.17 In cattle, iodine deficiency leads to marked induction of selenoprotein-D1, accompanied by elevated glutathione peroxidase (GPX) activity. Finally, diets containing adequate levels of crude protein and cellulose can enhance animal’s ability to absorb and utilize Se more efficiently.

Selenium intake without supplementation

Most Se for beef cattle is obtained through forage, with soluble Se compounds in water a much poorer source.15 In areas with moderately low or variable soil Se concentrations, certain plants, (e.g. alfalfa) incorporate more Se than other forages (e.g. red clover, timothy, or brome grasses).18 Therefore, feeding alfalfa in these regions can reduce the need for supplementation. Additionally, neutral or acidic soils can impair a plant’s ability to uptake Se. Forage testing is an important tool in evaluating herd Se status.19

Organic Se compounds in plant matter are easily absorbed by the gastrointestinal tract and have more prolonged retention. In contrast, inorganic Se (e.g. selenate) in water is readily absorbed but also rapidly excreted. Excess Se is primarily excreted in urine, with lesser amounts excreted in feces and breath. Selenium is mainly stored in the liver and, to a lesser extent, in the kidney.19

Selenium utilization

Selenium is present in nearly all tissues, but it is most concentrated in tissues that are rapidly breaking down, growing, or dividing, including heart, skeletal muscle, ovaries, and testes. It is also present in immune system tissues (including bone marrow, thymus, liver, intestines, spleen, and lymph nodes), thyroid, and other organs.20 There are many selenoproteins, each with a specific location and function. Selenoproteins involved in reproduction are listed (Table 1).21,22

Table 1. Selenoproteins, principal location, and functions
Nomenclature Selenoprotein Location Function
GPX1 Glutathione peroxidase 1 Follicle Antioxidant protection
GPX2 Glutathione peroxidase 2 Embryo Antioxidant protection
GPX3 Glutathione peroxidase 3 Follicle, endometrium Antioxidant protection
GPX4 Glutathione peroxidase 4 Embryo, testis, sperm mitochondrial sheath Antioxidant protection
GPX5 Glutathione peroxidase 5 Epididymis, sperm Antioxidant protection
TXNRD1 Thioredoxin reductase 1 Embryo Antioxidant role, redox regulation, cell signaling
TXNRD2 Thioredoxin reductase 2 Embryo Antioxidant role, redox regulation, cell signaling
TXNRD3 Thioredoxin-glutathione reductase Sperm Antioxidant role, redox regulation, cell signaling
DIO1,2 &3 Iodothyronine deiodinase 1, 2, and 3 Utero-placental unit T3 production
SELENOH Selenoprotein H Trophoblast, placenta Glutathione synthesis
SELENOP Selenoprotein P Seminal plasma, utero-placental unit Se transport, antioxidant
MCSeP Mitochondrial selenoprotein Sperm mitochondrial capsule Store for GPX4
TGR Thioredoxin-glutathione reductase Spermatid Antioxidant

Selenium has a crucial role as a functional component of a group of antioxidants known as GPX,23,24 a water-soluble cytosolic enzyme that protects cellular membranes and membranes of lipid-containing organelles, from irreversible damage caused by peroxides. Vitamin E has a similar function, but as a lipid-soluble antioxidant in cell and organelle membranes. Peroxides can denature cellular proteins, causing cell degeneration and death. Glutathione peroxidase catalyzes breakdown of hydrogen peroxide (H2O2) and related hydroperoxides.23,24 Based on a cell membrane as the central structure, the role of oxidative stress (OS), generation of reactive oxygen species (ROS), antioxidant defenses, and lipid peroxidation are summarized (Figure 3).

Figure 3.
Figure 3. Schematic presentation of cell membrane oxidative metabolism/antioxidant interactions, indicating how GPX 1, 2, and 4 and other micronutrients protect membranes and organelles from peroxidation23,27

Cell membrane and phospholipids

The cell membrane’s phospholipid bilayer, with hydrophilic heads and hydrophobic tails, maintains membrane integrity and selective permeability.25 Unsaturated fatty acids in the tails create bends that promote fluidity, crucial for membrane flexibility, protein movement, and communication. Lipid peroxidation from ROS damages the membrane, triggering inflammation and cell death if uncontrolled.26

Reactive oxidative stress generation

Mitochondria are the main source of ROS during ATP production, leaking electrons that form superoxide anions (O2•–), which convert to H2O2.28,29 NADPH oxidases and enzymes like cytochrome P450 and lipoxygenases also contribute to ROS production, particularly in immune responses and inflammation.30-32

Enzyme actions in reactive oxidative stress detoxification

Enzymes like GPX, superoxide dismutase (SOD), and catalase protect cells by neutralizing ROS. Glutathione peroxidase reduces lipid peroxides, SOD converts superoxides to H2O2, and catalase converts H2O2 to water and oxygen, preventing oxidative damage.27,33,34

Micronutrient protection against reactive oxidative stress

Vitamin E, a fat-soluble antioxidant, protects membrane lipids from oxidative damage.36,37,38 Vitamin C scavenges ROS and regenerates antioxidants,35,36 whereas CoQ10 neutralizes lipid-soluble ROS and supports mitochondrial function and ATP production.38

Oxidative stress and membrane damage

Oxidative stress occurs when ROS production exceeds antioxidant defenses, causing membrane damage, destabilizing fluidity, and impairing function.39 This can lead to protein dysfunction, increased permeability, and cell death.40 Antioxidants and membrane repair mechanisms help prevent and restore membrane integrity.

Role of selenium in immunity

Selenium has a crucial role in maintaining immune function and supporting defenses against infections. As a key antioxidant, it is integral to several cellular processes that regulate immune responses, particularly through its incorporation into enzymes like GPX that manages OS and inflammation.41 Given the close relationship between Se and vitamin E, it is not surprising that many Se-responsive diseases may also respond to vitamin E supplementation. Selenium’s role in the immune system is summarized below.

Cell-mediated and humoral immunity

Selenium, in conjunction with vitamin E, is essential for both cell-mediated and humoral immunity. Deficiencies in Se compromise resistance to infections, reduce neutrophil function, and decrease antibody production. These deficiencies affect proliferation of T and B lymphocytes in response to mitogens and impair the function of natural killer cells.42

Neutrophil function

Neutrophils have a key role in the innate immune response and rely heavily on Se to maintain high GPX enzyme activity.43 This enzyme is vital for managing OS during phagocytosis (process by which neutrophils engulf and kill pathogens). Without adequate Se, neutrophils have a reduced ability to eliminate pathogens and manage peroxides generated during this process.43,44

Selenium supplementation in colostrum significantly increased IgG concentrations in calves45; a single feeding of colostrum supplemented with 3.0 ppm Se caused a 40% increase in peripheral IgG that persisted at least 2 weeks, implying a prolonged benefit to immunity. Increases in IgG were attributed to Se’s ability to promote pinocytosis (the process by which cells absorb antibodies from colostrum) within intestinal epithelial cells.46 This mechanism ensures more efficient absorption of immunoglobulins, providing calves with better passive immunity.

Improved humoral response

Selenium supplementation enhanced the humoral immune response in cattle experimentally infected with the infectious bovine rhinotracheitis virus.47 Selenium-supplemented cattle produced more antibodies and had a stronger immune response compared to control groups.

Although Se deficiency may increase susceptibility to infections, naturally Se-deficient herds have not had a consistent increase in infection rates or severity.45,48 In addition to Se, other factors also influence disease incidence.

Selenium is transferred from dam to fetus during pregnancy, ensuring a calf is born with adequate Se. Prenatal Se supplementation in dams helps produce Se-sufficient calves and improves immune status at birth.49 After birth, Se concentrations in calves deplete rapidly, typically within 18 days. However, the initial boost in Se from the dam may provide early-life protection against neonatal morbidity and disease. Milk Se concentrations are highly correlated with maternal blood Se concentrations. Selenium-adequate dams can provide Se-sufficient milk to their calves until weaning, supporting calf’s immune system until they are able to consume solid feed.50,51 In cattle, Se supplementation can enhance passive immunity (IgG transfer), improve immune responses during infections, and provide essential nutrients to offspring through placenta and milk. Ensuring dams and calves are sufficient to promote a strong immune system, reduces susceptibility to infections and improves herd health.

Role of selenium in thyroid function

In cattle, Se has a critical role in thyroid function by supporting synthesis, metabolism, and regulation of thyroid hormones.52 Thyroid gland produces hormones, primarily thyroxine (T4) and triiodothyronine (T3) that regulate metabolism, growth, and development. Selenium is essential for enzymes involved in the activation and deactivation of these hormones. Selenium is incorporated into several selenoproteins that are crucial for thyroid function, most notably the deiodinase enzymes, in cattle, mice, and humans.52,53 These enzymes are responsible for the activation and inactivation of thyroid hormones:

Type 1 deiodinase: This enzyme converts T4 into the more active T3 that is essential for regulating metabolism and energy balance; it is highly active in liver and kidneys.

Type 2 deiodinase: This enzyme converts T4 to T3, but it is mainly active in the brain, pituitary, and brown adipose tissue. In the brain, it has an important role in regulating local concentrations of T3 to support neurodevelopment and cognition.

Type 3 deiodinase: This enzyme converts T4 and T3 to inactive forms; it has an important role in regulating thyroid hormone action, especially in placenta and brain.

In cattle, inadequate Se reduces the efficiency of these enzymes and the conversion of T4 into active T3.52

Antioxidant defense in the thyroid

Selenium is a key component of GPX, an enzyme that helps protect the thyroid from OS54 when it generates H2O2 during thyroid hormone synthesis. Excess H2O2 can cause oxidative damage to thyroid cells.55 Glutathione peroxidase, with the help of Se, neutralizes this peroxide, prevents damage and ensures thyroid function.54 The antioxidant role of Se protects the thyroid from damage during high hormone production or stress.

Thyroid hormone synthesis

Selenium is involved in synthesis of thyroid hormones; adequate Se concentrations ensure that the thyroid can produce sufficient T4 and T3.52,56 Although iodine is a key component for thyroid hormone synthesis, Se promotes thyroid function, contributing to activation of thyroid hormones. In cattle, selenium affects pituitary release of thyroid-stimulating hormone (TSH) that stimulates thyroid to produce T4 and T3.58 Further, Se deficiency can increase TSH concentrations to compensate for low thyroid hormone concentrations, potentially causing subclinical hypothyroidism (marginal thyroid hormone concentrations).57

Selenium deficiency and thyroid hormone imbalance

When Se concentrations are inadequate, the conversion of T4 to T3 is impaired due to reduced activity of the deiodinase enzymes; this can reduce the T3/T4 ratio that can affect various metabolic processes. A Se-deficient diet reduces T3 concentrations, although T4 concentrations may increase. This imbalance can lead to suboptimal metabolic function and growth issues, as T3 is the active hormone responsible for regulating energy expenditure, cell growth, and development.58 Selenium deficiency in calves is often associated with poor growth and performance,12,59 due in part due to reduced thyroid function and hormonal imbalance. Since T3 is involved in regulation of growth, Se deficiency could impair growth rates and developmental processes in young animals.1,12,59 Selenium-deficient calves often have slower growth rates, likely due to impaired thyroid function and reduced T3.12,59 In these calves, Se supplements can restore normal thyroid function, improve T3 production, and promote growth. However, Se supplementation typically does not affect growth in well-nourished calves.

Selenium supplementation and improved thyroid function

Milk selenium and neonatal growth

The correlation between milk Se concentrations and neonatal T3 concentrations highlights the importance of Se-rich milk for supporting newborn development. Since T3 has a critical role in growth, adequate Se intake during the neonatal period is essential for promoting growth and development in offspring.

Positive effects in ewes and lambs

Selenium supplementation can increase T3 in both ewes and their lambs. For example, Se-supplemented ewes had higher T3 in their serum and milk that positively affected thyroid hormone concentrations in their lambs. In these lambs, there was a strong positive correlation between milk Se concentration and serum T3 (r = 0.84, p < 0.01).60,61 In contrast, a negative relationship was observed in the control (unsupplemented) group; lower Se intake reduced T3 and increased the T4/T3 ratio.

Role in fetal development

Selenium transfer from dam to fetus

Selenium is primarily incorporated into selenoproteins (e.g. GPX and thioredoxin reductase) that have critical roles in reducing OS and protecting cells. The fetus relies on maternal Se to ensure proper development and to establish its own antioxidant defenses. Selenium is actively transported across the placenta from maternal blood to the fetus.62 The placenta has specialized transport systems to facilitate transfer of various nutrients and trace elements, including Se, to support fetal development. Selenium is transported in the blood as selenomethionine or selenate and transferred from dam to fetus via the placenta, facilitated by placental transporters, including sodium-dependent active transport mechanisms.63,64 Fetal Se concentrations largely depend on maternal Se intake.62,64 If a dam has adequate Se, the fetus is typically well supplied. However, maternal Se deficiency can reduce Se transfer to the fetus, with detrimental effects on fetal development.65 Selenium, through its role in selenoproteins (GPX), protects fetal tissues from oxidative damage, crucial during rapid cell division and organ development.66

Selenium’s role in embryonic development and maternal health is critical, especially during pregnancy, where it influences antioxidant defense, hormonal regulation, and fetal growth.66-68 Although much of Se’s function is understood in terms of postnatal development, its importance during pregnancy is equally important, particularly in protecting the fetus from OS and supporting placental function. The role of Se in embryonic development, fetal health, and maternal nutrition during pregnancy is as follows:

Selenium’s role in embryonic development and antioxidant protection

Selenium and pregnancy complications

Figure 4.
Figure 4. Roles of selenium in female reproduction

Placental development and selenium’s influence on oxidative balance

Effects of selenium supplementation on maternal health and fetal development

Effects on lactation and offspring growth

Selenium is vital for supporting healthy fetal development, placental function, and maternal health during pregnancy. Its role in reducing OS and supporting hormone production is indispensable to support pregnancy and promote growth and development of the offspring.

Role in female reproduction

Selenium offers a broad range of health benefits for livestock, especially cattle, having a crucial role in reproductive health. Deficiencies in Se can cause large economic losses, due to impaired fertility, increased incidence of mastitis, metritis, RFM, and others.13,84

Selenium has a vital role in oocyte and ovary function. In an in vitro study using a buffalo oocyte cell line, Se significantly improved the rate of nuclear maturation and reduced the number of cells in the germinal vesicle stage. Although Se did not affect cell development at other meiotic stages, it altered expression of several genes involved in oocyte development, including downregulating Casp3 and Amh, and upregulating GPX4 and SOD.85 Selenium also reduced transcript levels of Pla2g3, a phospholipase involved in lipid metabolism.85,86 Similarly, in a study on primary luteinized granulosa cells from goat ovarian follicles, Se stimulated cell proliferation and increased markers associated with estradiol production, such as 3β-HSD, p-Akt, cAMP, and steroidogenic acute regulatory protein.87 Therefore, Se may regulate the hypothalamic-pituitary-gonadal (HPG) axis by influencing sex hormone production through its effects on redox balance and lipid metabolism.

In terms of reproductive health, Se is critical for fertility and early embryonic development. Adequate Se reduces OS during ovarian follicular and CL development, thereby protecting reproductive organs from ROS (Figure 4).77 Selenium also has a key role in maintaining progesterone production in heifers that is essential for pregnancy maintenance (Figure 4).77 Without sufficient Se, the CL cannot function properly that can lead to reproductive failure. Selenium supplementation reduces the incidence of RFM, metritis, endometritis, and ovarian cysts, all negatively affect cow health and herd productivity. Ensuring Se adequacy before and after calving is crucial to optimize reproduction.88-91 Cows with adequate Se also have fewer services per conception, a higher pregnancy rate at first service, and a shorter interval to conception,90,91 all improve reproductive efficiency.

Selenium also impacts mastitis and metritis. Selenium deficiency can impair milk quality, alter colostrum composition, and hinder immune transfer to the offspring.81,92-97 Inadequate Se increases the risk of mastitis.98 Selenium’s antioxidant properties protect the mammary gland from oxidative damage, reducing mastitis incidence (Figure 4).99 Selenium supplementation also reduces the risk of metritis, a uterine infection that can follow calving13,91 and lead to prolonged postpartum anestrus, delaying conception. By improving immune function and reducing inflammation, Se helps prevent these conditions, enhancing reproductive health.100,101

Regarding Se supplementation sources, the form of Se (sodium selenite or selenized yeast) has little impact on conception rates or calving intervals.102 However, sources may vary in bioavailability and effectiveness in various farming systems. Regardless of the source, ensuring adequate Se in the diet is essential for maintaining overall reproductive health in cattle.

From an economic perspective, Se supplementation improves reproductive efficiency by reducing the number of services per conception, improving first-service success rates, and shortening calving intervals.103 These benefits increase herd productivity and profitability. Selenium also lowers the incidence of metritis, mastitis, and RFM, reducing veterinary costs and leading to healthier cows1,56,88,103 with greater milk yields, longevity, and long-term profitability.

Further, the bovine ovary contains high levels of Se that are localized to healthy preovulatory follicles, but not atretic follicles.72 The presence of Se in healthy follicles implies involvement in preparing the oocyte for fertilization, embryo development, and postnatal life (Figure 4). Adding Se to in vitro fertilization (IVF) cultures for cattle, dogs, pigs, and yaks improved embryo development, reduced ROS, and decreased DNA damage.104-108 Cattle fed organically bound Se have better conceptus length and differential expression of genes related to pregnancy recognition (Figure 4).109,110 Furthermore, ewes supplemented with Se throughout pregnancy have increased cell density and cell proliferation in the placenta during late pregnancy that correlates with improved lamb birth weights.111 These effects on placental development may partially explain effects of Se on fetal growth and development.111-114 In humans, low Se in plasma, follicular fluid, or amniotic fluid, as well as low tissue GPX, are associated with infertility, miscarriage, preterm birth, gestational diabetes, and SGA fetuses,75,115-118 emphasizing the importance of Se for reproductive success across species.

1. Regulates preantral and preovulatory follicle function, enhancing fertility competence of oocytes; 2. Enhances CL function, ensuring sufficient progesterone to support pregnancy; 3. Promotes successful fertilization; 4 and 5. Improves early embryonic development in the oviduct by increasing the cleavage rate and 8-cell embryo development; 6. Enhances blastocyst rate; 7 and 8. Increases conceptus length by enhancing the expression of genes related to maternal recognition of pregnancy, including interferon-stimulated genes and progesterone-stimulated genes; 9. Promotes early embryo and fetal development; 10. Increases cell density and cell proliferation in the placenta; 11. As the placenta is the primary site for the exchange of nutrients, respiratory gases, and metabolic wastes, Se promotes fetal growth and development; 12. Protects mammary gland from oxidative damage and reduces incidence of mastitis; 13. Enhances immune function in neonate.

Selenium is an essential micronutrient that has a crucial role in immune function and reproductive health in cattle. It helps protect against OS and inflammation, supports fertility, and improves milk quality. Supplementing cattle with Se, especially in areas where the soil is deficient, can improve reproductive efficiency, health outcomes, and overall economic performance. Ensuring adequate Se before and during pregnancy, as well as in the postpartum period, can significantly reduce the incidence of reproductive disorders such as RFM, metritis, and ovarian cysts, while also enhancing immune function and disease resistance.

Role in male reproduction

Selenium has a crucial role in sperm health, sperm parameters and fertility,119 particularly in bulls (Figure 5). Selenium, through its incorporation into selenoproteins like GPX4,120 has several protective and structural functions in sperm, promoting viability, motility, and integrity that are critical for fertility. Selenium is an essential component of GPX4, a key antioxidant enzyme protecting sperm from oxidative stress-induced damage.119 Selenium (via GPX4) contributes to the structural integrity of the sperm’s midpiece, critical for mitochondrial function and motility.121 Oxidative stress caused by ROS can damage sperm membranes and impair motility.122 Adequate Se protects sperm mitochondria producing energy that is essential for sperm motility.123,124 Poor motility reduces sperm fertilizing ability and fertility.

Figure 5.
Figure 5. Effects of selenium supplementation on sperm and fertility

Although GPX4 activity is not significant in sperm, it is crucial for protecting sperm at various stages of development. In the early stages of spermatogenesis, GPX4 protects sperm DNA from oxidative damage. GPX4 is strongly expressed in seminiferous tubules of healthy bulls, particularly in spermatogonia, round spermatids, and elongated spermatids, suggesting a critical role in sperm maturation. Immuno-signals for GPX4 are also detected in the acrosomal region of epididymal and ejaculated sperm, further emphasizing its importance in sperm function.119

Impact on sperm quality

Selenium supplementation of Holstein bulls improved various sperm quality parameters, including viability, motility, membrane integrity, and postthaw quality. These improvements are particularly notable after semen cryopreservation.125 Supplementation also reduced lipid peroxidation and apoptosis/necrosis rates in sperm that are commonly associated with oxidative damage. Selenium supplementation elevates antioxidant biomarkers in seminal plasma, including total antioxidant capacity (TAOC) and malondialdehyde (MDA), markers of OS. Selenium reduces oxidative damage to the sperm, particularly in winter and autumn, when GPX concentrations in the testes naturally increase.126 Selenium deficiency can increase abnormal sperm morphology (e.g. deformed heads or tails) that reduces fertilizing ability.127 Selenium, through its antioxidant properties, helps prevent oxidative damage to sperm DNA that is crucial for fertilization and development.128

Selenium has a multifaceted role in protecting sperm from oxidative damage, improving sperm quality, and contributing to overall fertility and reproductive health in bulls. By incorporating Se into selenoproteins (e.g. GPX4), sperm maintain structural integrity, motility, and viability, making Se supplementation a useful tool for improving sperm health and fertility.

Selenium nanoparticles (SeNPs) protect against aflatoxin B1 induced toxicity, reducing morphologically abnormal sperm and DNA fragmentation129 and preserving testicular architecture, mitigating atrophy of the seminiferous tubules.130 Furthermore, SeNPs protected against deltamethrin-induced reproductive toxicity and negative effects such as sperm characteristics, TST, and antioxidant biomarkers, as well as behavioral and histopathological alterations. Bulls given SeNPs had improved semen parameters, antioxidant status, and sexual performance.131 In addition, SeNPs improved the quality of semen in rats and goats.131-133

Selenium’s role in testosterone production

Hormonal regulation: Selenium has an indirect but essential role in testosterone (TST) production by supporting testicular function. Testosterone is a key hormone for spermatogenesis and overall bull fertility.

Selenium and the hypothalamic-pituitary-gonadal axis: Selenium is involved in the proper functioning of the HPG axis that regulates the release of hormones, including LH and Follicle stimulating hormone (FSH).134 These hormones stimulate the testes to produce TST and sperm. Selenium also helps regulate the enzymes involved in testicular function.

Selenium is also important for maintaining production of sex steroid hormones, including TST, estradiol, and progesterone. Selenium depletion lowered TST concentrations while decreasing testicular mass and adversely affecting testicular morphology.135 Although testicular mass of first-generation selenium-deficient rats was not significantly changed, each successive generation had increasingly worsening symptoms. Exogenous GnRH or LH induced a reduced TST secretion in Se-deficient rats; perhaps TST production was impaired or receptors or signaling pathways for GnRH and LH were affected. Selenium supported TST synthesis by activating the extracellular signal-regulated kinase (ERK) signaling pathway in ovine Leydig cells.136

Selenium affects proliferation and apoptosis of Leydig cells by regulating OS and expression of cell cycle and apoptosis-related genes.131,132 In addition, Se can enhance TST production by activating the ERK signaling pathway and expression of downstream genes (StAR and 3β-HSD) that could be related to regulatory roles of Se in male fertility and spermatogenesis.136,137

Selenium has an important role in immune system function, enhancing the ability of white blood cells (e.g. neutrophils and lymphocytes) to respond to infections.133 A healthy immune system is crucial for maintaining reproductive health in bulls, as it reduces risk of reproductive infections (seminal vesiculitis, epididymitis, or orchitis) that can impair sperm production and quality.138 Selenium deficiency can suppress immune responses, increasing susceptibility to reproductive tract infections that reduce sperm quality.

Seminal plasma

Selenium is present in the seminal plasma (457.4 ± 108.7 μg/liter) and its antioxidant activity protects sperm from oxidative damage during ejaculation and transport through the female reproductive tract.136,137 Selenium is also involved in production of seminal plasma proteins that support sperm viability and function. Selenium-dependent enzymes promote the health of sperm and improve their ability to survive in the female reproductive tract.

Fertility and in vitro findings

Selenium supplementation enhances sperm function in IVF. It significantly improves mitochondrial activity in sperm and sperm acrosome integrity and promotes sperm binding to the zona pellucida (ZP), critical for fertilization.21,139

Beef cattle selenium requirements

Concentrations of blood Se > 100 mg/liter are required to maintain optimum immunocompetence in growing beef cattle.140 Dietary requirements to avoid NMD are 0.1 mg/kg DM. Regular Se analysis of forages and feeds is necessary to detect deficiencies, and supplementation may be needed, in the form of salt blocks, loose minerals, or selenium-enriched yeasts.3 The FDA permits selenium to be included in the total diet of beef cattle at a maximum level of 0.3 ppm of dry matter. In areas where deficiencies are common, the maximum allowable level should be used (https://www.ecfr.gov/current/title-21/chapter-I/subchapter-E/part-573/subpart-B/section-573.920 [cited April 8 2025]). Additionally, the FDA allows up to 120 ppm of Se to be incorporated into a salt-mineral mixture for free-choice feeding. Selenium deficiency is unlikely if adequate amounts are consumed through the mineral supplement. However, the Se concentration in the supplement and the labeled intake must ensure that the total daily intake does not exceed 3 mg. For example, a mineral supplement with a recommended intake of 4 ounces per head per day cannot contain more than 26 ppm of Se.

Clinical presentation of selenium deficiency in various age groups

Selenium deficiency, often paired with a lack of vitamin E, can lead to various NMD in cattle, with clinical signs that can range from acute to subacute.141 These disorders affect a wide array of conditions, including poor growth in pastured calves, lowered milk production and subclinical mastitis in dairy cows, decreased fertility, embryonic death, RFM, metritis, poor uterine involution, cystic ovaries, impaired immune function, and even premature death, especially in cases of marginal Se deficiency.3

In neonates, Se is crucial for fetal development, and its deficiency in calves can lead to severe health issues, as Se crosses the placenta from dam to fetus. Selenium-deficient calves may suffer from myocardial necrosis, heart failure, and other systemic issues due to insufficient antioxidant activity from GPX, an enzyme dependent on Se. Clinical signs include premature birth, perinatal death, heart or respiratory failure, and spontaneous abortion. Postmortem findings will typically include myocardial and skeletal muscle damage. Timely Se supplementation to both dams and calves is essential for preventing further damage.8,20

In beef calves aged 2-8 months, Se deficiency often manifests as acute or subacute NMD after unaccustomed exercise. Calves raised indoors and then exposed to pastures or those moved long distances may develop NMD due to Se-deficient diets. The OS from exercise accelerates muscle degeneration, leading to muscle calcification and widespread tissue damage. Acute NMD can lead to death from heart failure or respiratory distress, with affected calves being weak, recumbent, and unable to stand.8,141 Subacute NMD, more common in rapidly growing calves, typically affects skeletal muscles, causing weakness and tremors but often resolves with treatment.3,142 Muscle degeneration releases several enzymes, including creatinine kinase (CK); this can be useful in supporting a diagnosis of NMD.1,136 Subclinical Se deficiency in older calves may manifest as ill thrift, with stunted growth, poor coat condition, and poor nutrient absorption, potentially leading to death.1,20

Yearling cattle, particularly those raised on Se-deficient diets or grain-based feeds that cause vitamin E degradation, are also susceptible to NMD.3 Subclinical cases often present as weakened immune systems, with an increased susceptibility to diseases like respiratory infections. Subacute NMD in yearlings can cause muscle degeneration, similar to clinical signs in older calves. Severe cases may lead to ‘flying scapula’143 or a spreading of toes, and muscle weakness may impair feeding or swallowing.1 Acute cases can cause myoglobinuria, stiffness, and even sudden death.3 Selenium supplementation alleviates some clinical signs, especially in beef steers, where it can improve prolactin and mitigate fescue toxicosis.144-149

In adult cattle, Se deficiency often manifests as reproductive issues, due to its crucial role in follicular development, progesterone production, and antioxidant defense during high metabolic stress (e.g. pregnancy and lactation). A Se-deficient herd may have higher rates of RFM, infertility, metritis, cystic ovaries, and early embryonic death, even with marginal deficiencies.3,20,150 Bulls are also affected, with reduced sperm motility and viability due to impaired selenoproteins in sperm tails and acrosomes, leading to decreased fertility.124,125

Selenium toxicosis

Selenium deficiency is more common than toxicosis, but the latter does occur. Mining operations can expose Se-bearing elements to air and water, mobilizing Se into aquatic systems where it bioaccumulates in the ground water, soil, grasses and forages, amplifying hazardous effects.151 Selenium toxicosis occurs when an animal’s diet exceeds 3-8 ppm of Se (threshold varies by species).152 Some animals can tolerate higher concentrations. Forage plants that lead to toxicosis typically contain 30-160 times the amount of Se required for nutrition. Poisoning can also result from consuming grains with elevated Se, affecting livestock such as poultry and swine.152

Selenium poisoning is classified into acute and chronic forms.153,154 Acute poisoning typically results from short-term ingestion of highly seleniferous plants, particularly when animals are hungry and consume low-palatable plants with high Se content. Symptoms of acute poisoning include abnormal posture, unsteady gait, abdominal pain, and, in severe cases, death.153,154 Chronic selenosis is associated with hair and hoof abnormalities. Bilateral alopecia or hair fragility and breakage along the mane, tail, and the nape are described in production animals. Chronic Se poisoning is further categorized into alkali disease and blind staggers.153,154 Alkali disease occurs when animals consume seleniferous forages (typically 5-40 ppm of Se) over extended intervals. Symptoms of alkali disease include dullness, emaciation, rough coats, hair loss, and lameness. Blind staggers result from grazing Se indicator plants containing water-soluble Se, with impaired vision, weakness, paralysis, and death from respiratory failure.

There is debate whether blind staggers is caused solely by Se, with other factors or toxins in plants suspected as having a role.155 Similar symptoms have been observed in conditions such as forage poisoning in Colorado, tansy mustard poisoning in the Southwest, and kochia poisoning.156 High sulfate concentrations in water or feed may also contribute to these symptoms, implying blind staggers may have multiple causes. Ultimately, alkali disease appears to be the primary chronic manifestation of Se poisoning, whereas blind staggers remain a more ambiguous condition that could involve additional toxins or unknown factors.

Reproductive effects of Se toxicity

Selenium toxicity can negatively affect reproduction in cattle in several ways. At higher concentrations, Se can become prooxidant, leading to OS and damage to cellular components. Elevated Se can impair sperm quality157 in bulls. Selenium controls development of granulosa cells and biosynthesis of estradiol-17β in adult ovaries in vitro.158 Selenosis can disrupt oocyte development leading to reduced fertility. High Se concentrations can cause spontaneous abortions, particularly in later stages of pregnancy.159 Calves born to cows with high Se exposure may have birth defects, particularly musculoskeletal issues.160 Selenium toxicity can decrease milk yield, possibly due to damage to mammary tissue or an overall decline in health.

Diagnosis of selenium deficiency

Testing soil, feed, and live cattle

If herd problems are primarily reproductive, general unthriftiness or subtle and deficient Se status is suspected, a diagnosis is typically made based on clinical signs and response to Se therapy. Testing is an important adjunct for diagnosis and is vital for future supplementation planning. Deficient, marginal, and normal Se concentrations standards for the analysis of different samples are provided (Table 2). Representative analysis of pasture/forage/herd samples are critical.

Table 2. Selenium concentration standards: deficient, marginal, and normal levels for various sample analyses
Sample types for testing Selenium level
Deficient Marginal Normal
Soil 0.5 mg/kg - -
Pasture < 0.02 mg/kg DM of pasture - Forages and grains with 0.1 mg/kg DM are considered adequate3
Serum† 0.002-0.025 mg/ml 0.03-0.07 mg/ml 0.08-0.3 mg/ml3
Whole blood‡ < 0.05 ppm 0.05-0.1 ppm > 0.11 ppm*
Serum erythrocyte GPX activity** 0.2-10 10-19 19-36
Serum CK levels*** - - 21-31 IU/L§
Liver biopsy 0.07-0.6 mg/ gram DM 0.45-0.9 mg/ gram DM 0.9-1.75 mg/ gram DM3

†It responds more rapidly to Se treatment than whole blood Se;
‡There is a delayed response to Se treatment compared to serum Se;
*(> 5 ppm high; Se toxicity)20
**This test is faster and more economical than testing for Se directly; however, the enzyme is unstable, and improper handling can significantly skew the results. The units are expressed as micromoles per minute at 37°C per gram of hemoglobin;
***It is the most common diagnostic aid for NMD, though it is not specific to Se deficiency syndromes. Its half-life is 2-4 hours, rapidly declining after myodegeneration, but it can remain elevated for up to 3 days following unaccustomed exercise. Levels typically return to normal within a few days of treatment;
§After a myodegeneration event, levels are commonly > 5,000-10,000 IU/liter3.

Diagnosis of selenosis

Diagnosis generally involves observation of symptoms such as hoof abnormalities, hair loss, and reproductive problems.161,162 Blood, serum samples or liver tissues are tested for Se.163 Normal Se concentrations in cattle are generally 0.05-0.10 ppm, with > 0.25 ppm considered toxic. Testing for Se content in the forage and feed is also critical.164 Liver and kidney are the most common postmortem samples used for Se analysis.165

Postmortem testing

Necropsy should be done on aborted fetuses or acute deaths, especially if NMD is suspected. The earlier the diagnosis and intervention, the more subclinical and subacute cases can be remedied. Because NMD is not an inflammatory process but rather degeneration of hyaline followed by coagulation necrosis +/- mineralization, there will be no muscle inflammation.1 No specific skeletal muscle is always affected, but groups of muscles are always affected bilaterally and symmetrically. They contain localized degenerative and necrotic areas that are white to gray. The affected area is often a streak through the center of an otherwise normal muscle or may be flanking either side of a normal piece of muscle.3

Diaphragm also has a streaked appearance but in a radiating pattern with a central focus of muscle degeneration/necrosis. The diaphragm will be very friable and edematous, with or without mineralization.3 If the muscles of the throat or chest are affected, secondary pneumonia is common.3 In calves with myocardium degeneration, the endocardium of the left ventricle is commonly affected. White to gray lesions may extend to involve interventricular septum and papillary muscles. Pulmonary congestion and edema are common with heart involvement.3

Treatment of selenium deficiency

Due to the close relationship vitamin E and Se in protecting cells and having difficulties in determining, which is the primary deficiency, Se and α-tocopherol combinations are recommended.3

Treating NMD is calves is best done with an injectable Se (3 mg) and DL alpha-tocopherol acetate (150 IU/ml) injection at 2 ml/45 kg BW IM. Once is usually sufficient unless it is the acute myocardial form where mortality can reach 90%. If there is at least 1 case of Se deficiency, treatment of the entire herd is recommended. As unaccustomed exercise is a predisposing factor for clinical NMD, cattle should be carefully handled during treatment. Subacute cases of NMD should improve by 3 days and regain mobility within 1 week.3

Treatment of selenosis

If Se toxicity is suspected, stop the use of any Se-containing feed supplements. In recovering steers, half-lives for Se elimination from serum, whole blood, liver, and muscle were 40.5 ± 8.2, 115.6 ± 25.1, 38.2 ± 5.0, and 98.5 ± 19.1 days, respectively (relatively long).166 Treatment may involve fluids, antioxidants, and liver-protective substances, but recovery can be slow, and severe cases may have permanent damage.167 Medications or supplements like vitamin E and antioxidants may reduce OS in the liver.

Preventing selenium deficiency with routine mineral supplementation

Selenium supplementation needs to be tailored to each specific operation. Current Se status must be known to determine how and when to supplement the herd.168 First, determine if the area in question is considered Se deficient; this can be gained from local extension offices or the US Geological Survey website.5 Consider testing pasture or feed and check labels of any packaged products.152 Are there any signs of Se deficiency, as described above? If so, consider blood testing for serum Se concentrations, whole-blood Se concentrations, or erythrocyte GPX concentrations, on a representative sample or all cattle.168

When developing a supplementation program, consider economics and logistics. There are inorganic and organic forms of Se. The inorganic form is usually sodium selenite that gives a short-duration increase in Se but does not persist. However, if applied to soil, it is readily taken up by plants and incorporated as organic Se. Organic Se is usually selenomethionine and typically provides a long-standing boost in Se status.168

Selenium injections, typically paired with vitamin E or copper, utilize inorganic sodium selenite, and are therefore best used as prevention in young livestock. In heifers and cows, injecting a Se and vitamin E supplement 3 weeks before calving can greatly decrease fertility problems, RFM, poor uterine involution, and cystic ovaries.3

Oral Se supplementation during pregnancy provides protection for the fetus due to placental transfer and may decrease neonatal morbidity and mortality. Selenium concentrations in colostrum and milk reflect the dam’s Se status. However, milk Se concentrations decrease 7 days after calving, so treatment of calves is often needed.3

Mineral supplementation is commonly used, typically in loose or block form. Loose is more common as it is more readily consumed, but Se can be leached by rain. Due to individual differences in intake and potential losses due to rain, results are often inconsistent.169

For calf NMD prevention, loose salt and mineral mix can be fed ad libitum. The recommended 0.1 mg/kg Se and 1 gram/day/head alpha-tocopherol can be achieved with 14.8 mg/kg of mixture and 2,700 IU/kg mixture of vitamin E. Cow and calf health and productivity are optimized by using this for the last 2 trimesters of pregnancy and first month of lactation.3,169

Fortified feed supplements have inorganic and/or organic sources of Se; the latter will produce a more prolonged increase in blood and liver Se concentrations than the former. Furthermore, organic sources result in more consistent intake on an individual basis.167 Seleno-yeast is an excellent option for supplementation in beef cattle. In pregnant cattle, seleno-yeast increased GPX activity better than sodium selenite when offered as a free-choice mineral.3 Selenium pellets are available as 10% Se and 90% iron grit. They can increase GPX activity for > 2 years and are effective when fed to pregnant cows in the last 3 months of pregnancy, increasing Se milk content to prevent calf NMD.3 These pellets were also used for growing cattle and did not cause toxicosis at 2-4 times the recommended dose. Alternatively, to ensure no problems upon turn out to pasture in the spring after being fed hay, straw, or high-moisture grain through the winter, supplementing with 0.1 mg/kg DM Se and 150 mg/day/head alpha-tocopherol can be used.3 Selenium boluses are only approved in California. They provide a consistent amount of Se that is slowly released from the bolus into the rumen, making them a good option for grazing animals where supplementation is not feasible.69 These supplementation options should be used year-round in Se-deficient areas to improve reproductive and immune health.

Agricultural practices can also increase soil Se concentrations, though they very rarely make a large impact. Applying manure of farm animals fed imported Se-adequate feed can slowly increase soil concentrations, although this can be a lengthy and expensive process.3 Finally, there are licensed products to fertilize Se-deficient soils. It is typically recommended to fertilize 5-10 grams of actual Se per acre; an application rate of 12-24 grams of sodium selenate per acre will provide the recommended 5-10 grams of actual Se per acre.167

Prevention of selenosis

Ensure that Se supplementation is done within the recommended levels; total Se intake for cattle should not exceed 0.3 mg/kg body weight per day. Regularly test forage and pasture soil for Se content,170 especially in areas known to have Se-rich soils. Forage or feed that contains 2-5 ppm Se poses a marginal threat to livestock. Forage with > 5 ppm Se will cause acute toxic conditions in livestock and should be avoided.170 High Se forage can be mixed with low Se forages to balance total Se content.171 In seleniferous areas with high Se concentrations, cattle should not be allowed to drink water with a Se concentration > 0.5 ppm.170

Conclusion

Selenium is a critical micronutrient with an indispensable role in cellular function; therefore, its importance cannot be overstated. Selenium, a powerful antioxidant, supports a variety of physiological processes, including immune function, thyroid hormone metabolism, and reproductive health. In the northwestern US, where soil and forage Se concentrations can be low or highly variable, this nutrient is particularly important. Deficiencies in Se are common in these regions, making it essential to ensure that animal health and productivity are not compromised. Inadequate Se intake can reduce fertility and the immune response, increase susceptibility to infectious diseases, and compromise growth rates in calves. Furthermore, Se deficiency can lead to more severe conditions, including NMD and cause death. Therefore, it is crucial to thoroughly assess Se status of animals and the local environment to determine potential deficiencies. Understanding how Se concentrations in the soil, forage, and livestock affect herd health will enable targeted supplementation strategies that improve livestock productivity, enhance disease resistance, and ensure long-term sustainability. Well-informed, proactive approach to Se supplementation can prevent costly health issues and optimize herd performance.

References

1. Mehdi Y, Dufrasne I: Selenium in cattle: a review. Molecules 2016;21:545. doi: 10.3390/molecules21040545
2. Hansen D, Hathaway R, Oldfield JE: White muscle and other selenium-responsive diseases of livestock. BCH-3410, May 1993. Adapted from the Cattle Producer’s Library. Available from: https://smallfarms.oregonstate.edu/sites/agscid7/files/seleniumdiseases.pdf [cited 28 September 2023].
3. Radostits OM, Gay CC, Hinchcliff KW, et al: Diseases associated with nutritional deficiencies. In: Veterinary Medicine: A Textbook of the Diseases of Cattle, Sheep, Pigs, Goats, and Horses. 10th edition, London; Elsevier Saunders: 2007.
4. Oldfield JE: Historical perspectives on selenium. Nutr Today 2001;36,100-102. doi: 10.1097/00017285-200103000-00017
5. Selenium in Counties of the Conterminous States. Available from: https://mrdata.usgs.gov/geochem/doc/averages/se/usa.html [cited June 26 2023].
6. Neve J, Favier A: Selenium in medicine and biology. Berlin, New-York; De Gruyter: 1989.
7. Geological distribution. In: Selenium in Nutrition: Revised Edition. National Research Council (US) Subcommittee on Selenium. Washington, DC; National Academies Press (US): 1983. Available from: https://www.ncbi.nlm.nih.gov/books/NBK216733/ [cited 28 September 2023].
8. Xiao J, Khan MZ, Ma Y, et al: The antioxidant properties of selenium and vitamin E; their role in periparturient dairy cattle health regulation. Antioxidants (Basel) 2021;10:1555. doi: 10.3390/antiox10101555
9. National Research Council (NRC). Nutrient Requirements of Beef Cattle. 7th revised edition (Update 2000), Washington, DC, USA; National Academy Press: 1996.
10. National Research Council (NRC). Nutrient Requirements of Beef Cattle. 6th edition, Washington, DC, USA; National Academy Press: 1984.
11. Chauhan SS, Celi P, Ponnampalam EN, et al: Antioxidant dynamics in the live animal and implications for ruminant health and product (meat/milk) quality: role of vitamin E and selenium. Anim Prod Sci 2014;54:1525-1536. doi: 10.1071/AN14334
12. Zust J, Hrovatin B, Simundić B: Assessment of selenium and vitamin E deficiencies in dairy herds and clinical disease in calves. Vet Rec 1996;139:391-394. doi: 10.1136/vr.139.16.391
13. Spears JW, Weiss WP: Role of antioxidants and trace elements in health and immunity of transition dairy cows. Vet J 2008;176:70-76. doi: 10.1016/j.tvjl.2007.12.015
14. Harrison JH, Conrad HR: Effect of dietary calcium on selenium absorption by the nonlactating dairy cow. J Dairy Sci 1984;67:1860-1864. doi: 10.3168/jds.s0022-0302(84)81514-3
15. García-Vaquero M, Miranda M, Benedito JL, et al: Effect of type of muscle and Cu supplementation on trace element concentrations in cattle meat. Food Chem Toxicol 2011:49:1443-1449. doi: 10.1016/j.fct.2011.03.041
16. Neathery MW, Miller WJ, Gentry RP, et al: Influence of high dietary lead on selenium metabolism in dairy calves. J Dairy Sci 1987;70:645-652. doi: 10.3168/jds.S0022-0302(87)80054-1
17. Zagrodzki P, Nicol F, McCoy MA, et al: Iodine deficiency in cattle: compensatory changes in thyroidal selenoenzymes. Res Vet Sci 1998;64:209-211. doi: 10.1016/s0034-5288(98)90127-8
18. Anderson JW, Scarf AR: Selenium and plant metabolism. In: Robb DA, Pierpoint WS, editors. Metals and Micronutrients: Uptake and Utilization by Plants. New York; Academic Press: 1983. p. 241-275.
19. Public Health Statement Selenium [CAS#: 7782-49-2]. Agency for Toxic Substnaces and Disease Registry, September 2003. Available from: https://permanent.fdlp.gov/gpo29941/tp92-c1-b.pdf [cited 28 September 2023].
20. Spallholz JE, Boylan LM, Larsen HS: Advances in understanding selenium’s role in the immune system. Ann N Y Acad Sci 1990;587:123-139. doi: 10.1111/j.1749-6632.1990.tb00140.x
21. Qazi IH, Angel C, Yang H, et al: Role of selenium and selenoproteins in male reproductive function: a review of past and present evidences. Antioxidants (Basel) 2019;8:268. doi: 10.3390/antiox8080268
22. Qazi IH, Angel C, Yang H, et al: Selenium, selenoproteins, and female reproduction: a review. Molecules 2018;23:3053. doi: 10.3390/molecules23123053
23. Brigelius-Flohé R, Maiorino M: Glutathione peroxidases. Biochim Biophys Acta 2013;1830:3289-3303. doi: 10.1016/j.bbagen.2012.11.020
24. Takahashi K, Cohen HJ: Selenium-dependent glutathione peroxidase protein and activity: immunological investigations on cellular and plasma enzymes. Blood 1986;68:640-645. doi: 10.1182/blood.V68.3.640.640
25. van Meer G, Voelker DR, Feigenson GW: Membrane lipids: where they are and how they behave. Nat Rev Mol Cell Biol 2008;9:112-24. doi: 10.1038/nrm2330
26. Cordeiro RM: Reactive oxygen species at phospholipid bilayers: distribution, mobility and permeation. Biochim Biophys Acta 2014;1838:438-444. doi: 10.1016/j.bbamem.2013.09.016
27. Pei J, Pan X, Wei G, et al: Research progress of glutathione peroxidase family (GPX) in redoxidation. Front Pharmacol 2023;14:1147414. doi: 10.3389/fphar.2023.1147414
28. Murphy MP: How mitochondria produce reactive oxygen species. Biochem J 2009;417:1-13. doi: 10.1042/BJ20081386
29. Jena AB, Samal RR, Bhol NK, et al: Cellular Red-Ox system in health and disease: the latest update. Biomed Pharmacother 2023;162:114606. doi: 10.1016/j.biopha.2023.114606
30. Taylor JP, Tse HM: The role of NADPH oxidases in infectious and inflammatory diseases. Redox Biol 2021;48:102159. doi: 10.1016/j.redox.2021.102159
31.Veith A, Moorthy B: Role of cytochrome P450S in the generation and metabolism of reactive oxygen species. Curr Opin Toxicol 2018;7:44-51. doi: 10.1016/j.cotox.2017.10.003
32. Wisastra R, Dekker FJ: Inflammation, cancer and oxidative lipoxygenase activity are intimately linked. Cancers (Basel) 2014;6:1500-21. doi: 10.3390/cancers6031500
33. Wang Y, Branicky R, Noë A, et al: Superoxide dismutases: dual roles in controlling ROS damage and regulating ROS signaling. J Cell Biol 2018;217:1915-1928. doi: 10.1083/jcb.201708007
34. Heck DE, Shakarjian M, Kim HD, et al: Mechanisms of oxidant generation by catalase. Ann N Y Acad Sci 2010;1203:120-125. doi: 10.1111/j.1749-6632.2010.05603.x
35. Ryan MJ, Dudash HJ, Docherty M, et al: Vitamin E and C supplementation reduces oxidative stress, improves antioxidant enzymes and positive muscle work in chronically loaded muscles of aged rats. Exp Gerontol 2010;45:882-95. doi: 10.1016/j.exger.2010.08.002
36. Packer L: Protective role of vitamin E in biological systems. Am J Clin Nutr 1991;53(4 Suppl):1050S-1055S. doi: 10.1093/ajcn/53.4.1050S
37. Traber MG, Stevens JF: Vitamins C and E: beneficial effects from a mechanistic perspective. Free Radic Biol Med 2011;51:1000-1013. doi: 10.1016/j.freeradbiomed.2011.05.017
38. Silva SVE, Gallia MC, Luz JRDD, et al: Antioxidant effect of Coenzyme Q10 in the prevention of oxidative stress in arsenic-treated CHO-K1 cells and possible participation of zinc as a pro-oxidant agent. Nutrients 2022;14:3265. doi: 10.3390/nu14163265
39. Ayala A, Muñoz MF, Argüelles S: Lipid peroxidation: production, metabolism, and signaling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal. Oxid Med Cell Longev 2014;2014:360438. doi: 10.1155/2014/360438
40. Gaschler MM, Stockwell BR: Lipid peroxidation in cell death. Biochem Biophys Res Commun 2017;482:419-425. doi: 10.1016/j.bbrc.2016.10.086
41. Huang Z, Rose AH, Hoffmann PR: The role of selenium in inflammation and immunity: from molecular mechanisms to therapeutic opportunities. Antioxid Redox Signal 2012;16:705-743. doi: 10.1089/ars.2011.4145
42. Kiremidjian-Schumacher L, Stotzky G: Selenium and immune responses. Environ Res 1987;42:277-303. doi: 10.1016/s0013-9351(87)80194-9
43. Lee TJ, Nettleford SK, McGlynn A, et al: The role of selenoproteins in neutrophils during inflammation. Arch Biochem Biophys 2022;732:109452. doi: 10.1016/j.abb.2022.109452
44. Boyne R, Arthur JR: The response of selenium-deficient mice to Candida albicans infection. J Nutr 1986;116:816-822. doi: 10.1093/jn/116.5.816
45. Bates A, Wells M, Laven R, et al: Effect of an injectable trace mineral supplement on the immune response of dairy calves. Res Vet Sci 2020;130:1-10. doi: 10.1016/j.rvsc.2020.02.007
46. Kamada H, Nonaka I, Ueda Y, et al: Selenium addition to colostrum increases immunoglobulin G absorption by newborn calves. J Dairy Sci 2007;90:5665-5670. doi: 10.3168/jds.2007-0348
47. Reffett JK, Spears JW, Brown TT Jr: Effect of dietary selenium on the primary and secondary immune response in calves challenged with infectious bovine rhinotracheitis virus. J Nutr 1988;118:229-235. doi: 10.1093/jn/118.2.229
48. Panousis N, Roubies N, Karatzias H, et al: Effect of selenium and vitamin E on antibody production by dairy cows vaccinated against Escherichia coli. Vet Rec 2001;149:643-646. doi: 10.1136/vr.149.21.643
49. Hall JA, Bobe G, Vorachek WR, et al: Effect of supranutritional maternal and colostral selenium supplementation on passive absorption of immunoglobulin G in selenium-replete dairy calves. J Dairy Sci 2014;97:4379-4391. doi: 10.3168/jds.2013-7481
50. Pavlata L, Prášek, J, Podhorský A, et al: Selenium metabolism in cattle: maternal transfer of selenium to newborn calves at different selenium concentrations in dams. Acta Vet Brno 2003;72:639-646. doi: 10.2754/avb200372040639
51. Grace ND, Ankenbauer-Perkins KL, Alexander AM, et al: Relationship between blood selenium concentration or glutathione peroxidase activity, and milk selenium concentrations in New Zealand dairy cows. N Z Vet J 2001;49:24-28. doi: 10.1080/00480169.2001.36198
52. Awadeh FT, Kincaid RL, Johnson KA: Effect of level and source of dietary selenium on concentrations of thyroid hormones and immunoglobulins in beef cows and calves. J Anim Sci 1998;76(4):1204-1215. doi: 10.2527/1998.7641204x
53. Sabatino L, Vassalle C, Del Seppia C, et al: Deiodinases and the three types of thyroid hormone deiodination reactions. Endocrinol Metab (Seoul) 2021;36:952-964. doi: 10.3803/EnM.2021
54. Forcina GC, Dixon SJ: GPX4 at the crossroads of lipid homeostasis and ferroptosis. Proteomics 2019;19:e1800311. doi: 10.1002/pmic.201800311
55. Szanto I, Pusztaszeri M, Mavromati M: H2O2 metabolism in normal thyroid cells and in thyroid tumorigenesis: focus on NADPH oxidases. Antioxidants (Basel) 2019;8:126. doi: 10.3390/antiox8050126
56. Hosnedlova B, Kepinska M, Skalickova S, et al: A summary of new findings on the biological effects of selenium in selected animal species - a critical review. Int J Mol Sci 2017;18:2209. doi: 10.3390/ijms18102209
57. Vasilev R, Vasileva I, Yugatova N, et al: DAFS-25k impact on cattle’s thyroid hormonal status. BIO Web Conf 2020;17:00214. doi: 10.1051/bioconf/20201700214
58. Kobayashi R, Hasegawa M, Kawaguchi C, et al: Thyroid function in patients with selenium deficiency exhibits high free T4 to T3 ratio. Clin Pediatr Endocrinol 2021;30:19-26. doi: 10.1297/cpe.30.19
59. Rowntree JE, Hill GM, Hawkins DR, et al: Effect of Se on selenoprotein activity and thyroid hormone metabolism in beef and dairy cows and calves. J Anim Sci 2004;82:2995-3005. doi: 10.2527/2004.82102995x
60. Hefnawy AEG, Tórtora-Pérez JL: The importance of selenium and the effects of its deficiency in animal health. Small Rumin Res 2010;89:185-192. doi: 10.1016/j.smallrumres.2009.12.042
61. Hefnawy AE, Youssef S, Aguilera PV, et al: The relationship between selenium and T3 in selenium supplemented and nonsupplemented ewes and their lambs. Vet Med Int 2014;2014:105236. doi: 10.1155/2014/105236
62. Van Saun RJ, Herdt TH, Stowe HD: Maternal and fetal selenium concentrations and their interrelationships in dairy cattle. J Nutr 1989;119:1128-1137. doi: 10.1093/jn/119.8.1128
63. Nandakumaran M, Dashti HM, Al-Zaid NS: Maternal-fetal transport kinetics of copper, selenium, magnesium and iron in perfused human placental lobule: in vitro study. Mol Cell Biochem 2002;231:9-14. doi: 10.1023/a:1014426612180
64. Weiss WP, Colenbrander VF, Cunningham MD: Maternal transfer and retention of supplemental selenium in neonatal calves. J Dairy Sci 1984;67:416-420. doi: 10.3168/jds.S0022-0302(84)81318-1
65. Koller LD, Whitbeck GA, South PJ: Transplacental transfer and colostral concentrations of selenium in beef cattle. Am J Vet Res 1984;45:2507-2510. doi: 10.2460/ajvr.1984.45.12.2507
66. Ojeda ML, Nogales F, Romero-Herrera I, et al: Fetal programming is deeply related to maternal selenium status and oxidative balance; Experimental offspring health repercussions. Nutrients 2021;13:2085. doi: 10.3390/nu13062085
67.Pappas AC, Zoidis E, Chadio SE: Maternal selenium and developmental programming. Antioxidants (Basel) 2019;8:145. doi: 10.3390/antiox8050145
68. Duntas LH: Selenium and at-risk pregnancy: challenges and controversies. Thyroid Res 2020;13:16. doi: 10.1186/s13044-020-00090-x
69. Nogales F, Ojeda ML, Jotty K, et al: Maternal ethanol consumption reduces Se antioxidant function in placenta and liver of embryos and breastfeeding pups. Life Sci 2017;190:1-6. doi: 10.1016/j.lfs.2017.09.021
70. Agarwal A, Maldonado Rosas I, Anagnostopoulou C, et al: Oxidative stress and assisted reproduction: a comprehensive review of Its pathophysiological sole and strategies for optimizing embryo culture environment. Antioxidants (Basel) 2022;11(3):477. doi: 10.3390/antiox11030477
71. Hammami S, Morató R, Romaguera R, et al: Developmental competence and embryo quality of small oocytes from pre-pubertal goats cultured in IVM medium supplemented with low level of hormones, insulin-transferrin-selenium and ascorbic acid. Reprod Domest Anim 2013;48:339-344. doi: 10.1111/j.1439-0531.2012.02160.x
72. Wydooghe E, Heras S, Dewulf J, et al: Replacing serum in culture medium with albumin and insulin, transferrin and selenium is the key to successful bovine embryo development in individual culture. Reprod Fertil Dev 2014;26:717-724. doi: 10.1071/RD13043
73. Deluao JC, Winstanley Y, Robker RL, et al: Oxidative stress and reproductive function: reactive oxygen species in the mammalian pre-implantation embryo. Reproduction 2022;164:F95-F108. doi: 10.1530/REP-22-0121
74. Lewandowska M, Sajdak S, Lubiński J: The role of early pregnancy maternal selenium levels on the risk for small-for-gestational age newborns. Nutrients 2019;11:2298. doi: 10.3390/nu11102298
75. Meyer AM, Reed JJ, Neville TL, et al: Effects of plane of nutrition and selenium supply during gestation on ewe and neonatal offspring performance, body composition, and serum selenium. J Anim Sci 2010;88:1786-1800. doi: 10.2527/jas.2009-2435
76. Pieczyńska J, Grajeta H: The role of selenium in human conception and pregnancy. J Trace Elemen Med Biol 2015;29:31-38. doi: 10.1016/j.jtemb.2014.07.003
77. Kamada H, Nonaka I, Takenouchi N, et al: Effects of selenium supplementation on plasma progesterone concentrations in pregnant heifers. Anim Sci J 2014;85:241-246. doi: 10.1111/asj.12139
78. Wu F, Tian FJ, Lin Y: Oxidative stress in placenta: health and diseases. Biomed Res Int 2015;2015:293271. doi: 10.1155/2015/293271
79. Vornic I, Buciu V, Furau CG, et al: Oxidative stress and placental pathogenesis: a contemporary overview of potential biomarkers and emerging therapeutics. Int J Mol Sci 2024;25:12195. doi: 10.3390/ijms252212195
80. Schoots MH, Gordijn SJ, Scherjon SA, et al: Oxidative stress in placental pathology. Placenta 2018;69:153-161. doi: 10.1016/j.placenta.2018.03.003
81. Chen J, Zhang F, Guan W, et al: Increasing selenium supply for heat-stressed or actively cooled sows improves piglet preweaning survival, colostrum and milk composition, as well as maternal selenium, antioxidant status and immunoglobulin transfer. J Trace Elem Med Biol 2019;52:89-99. doi: 10.1016/j.jtemb.2018.11.010
82. Modzelewska D, Solé-Navais P, Brantsæter AL, et al: Maternal dietary selenium intake during pregnancy and neonatal outcomes in the Norwegian mother, father, and child cohort study. Nutrients 2021;13:1239. doi: 10.3390/nu13041239
83. Yang Z, Zheng Y, Ren K, et al: Hydroxy-selenomethionine helps cows to overcome heat stress by enhancing antioxidant capacity and alleviating blood-milk barrier damage. Anim Nutr 2024;20:171-181. doi: 10.1016/j.aninu.2024.10.003
84. Kommisrud E, Osterås O, Vatn T: Blood selenium associated with health and fertility in Norwegian dairy herds. Acta Vet Scand 2005;46:229-240. doi: 10.1186/1751-0147-46-229
85. El-Naby AAH, Ibrahim S, Hozyen HF, et al: Impact of nano-selenium on nuclear maturation and genes expression profile of buffalo oocytes matured in vitro. Mol Biol Rep 2020;47:8593-8603. doi: 10.1007/s11033-020-05902-9
86. Starkl P, Marichal T, Galli SJ: PLA2G3 promotes mast cell maturation and function. Nat Immunol 2013;14:527-529. doi: 10.1038/ni.2612
87. Yao X, Ei-Samahy MA, Fan L, et al: In vitro influence of selenium on the proliferation of and steroidogenesis in goat luteinized granulosa cells. Theriogenology 2018;114:70-80. doi: 10.1016/j.theriogenology.2018.03.014
88. Harrison JH, Hancock DD, Conrad HR: Vitamin E and selenium for reproduction of the dairy cow. J Dairy Sci 1984;67:123-132. doi: 10.3168/jds.S0022-0302(84)81275-8
89.Li H, Dong J, Wang Z, et al: Development potential of selenium in the prevention and treatment of bovine endometritis. Reprod Domest Anim 2024;59:e14647. doi: 10.1111/rda.14647
90. Aréchiga CF, Vázquez-Flores S, Ortíz O, et al: Effect of injection of beta-carotene or vitamin E and selenium on fertility of lactating dairy cows. Theriogenology 1998;50:65-76. doi: 10.1016/s0093-691x(98)00114-9
91. Wilde D: Influence of macro and micro minerals in the peri-parturient period on fertility in dairy cattle. Anim Reprod Sci 2006;96:240-249. doi: 10.1016/j.anireprosci.2006.08.004
92. Zhang S, Wu Z, Heng J, et al: Combined yeast culture and organic selenium supplementation during late gestation and lactation improve preweaning piglet performance by enhancing the antioxidant capacity and milk content in nutrient-restricted sows. Anim Nutr 2020;6:160-167. doi: 10.1016/j.aninu.2020.01.004
93.Sordillo LM: Selenium-dependent regulation of oxidative stress and immunity in periparturient dairy cattle. Vet Med Int 2013;2013:154045. doi: 10.1155/2013/154045
94.Eulogio GLJ, Hugo CV, Antonio CN, et al: Effects of the selenium and vitamin E in the production, physicochemical composition and somatic cell count in milk of Ayrshire cows. J Anim Vet Adv 2012;11:687-691.
95.Horký P: Effect of selenium on its content in milk and performance of dairy cows in ecological farming. Potravinarstvo 2015;9:324-329. doi: 10.5219/492
96.Ran L, Wu X, Shen X, et al: Effects of selenium form on blood and milk selenium concentrations, milk component and milk fatty acid composition in dairy cows. J Sci Food Agric 2010;90:2214-2219. doi: 10.1002/jsfa.4073
97. Juniper DT, Rymer C, Briens M: Bioefficacy of hydroxy-selenomethionine as a selenium supplement in pregnant dairy heifers and on the selenium status of their calves. J Dairy Sci 2019;102:7000-7010. doi: 10.3168/jds.2018-16065
98. Wang D, Jia D, He R, et al: Association between serum selenium level and subclinical mastitis in dairy cattle. Biol Trace Elem Res 2021;199:1389-1396. doi: 10.1007/s12011-020-02261-1
99. Wang H, Bi C, Wang Y, et al: Selenium ameliorates Staphylococcus aureus-induced inflammation in bovine mammary epithelial cells by inhibiting activation of TLR2, NF-κB and MAPK signaling pathways. BMC Vet Res 2018;14:197. doi: 10.1186/s12917-018-1508-y
100. Cui L, Zhang M, Zheng F, et al: Selenium elicited an enhanced anti-inflammatory effect in primary bovine endometrial stromal cells with high cortisol background. BMC Vet Res 2024;20:383. doi: 10.1186/s12917-024-04240-3
101. Cui L, Zheng F, Zhang M, et al: Selenium suppressed the LPS-induced oxidative stress of bovine endometrial stromal cells through Nrf2 pathway with high cortisol background. J Anim Sci 2024;102:skae260. doi: 10.1093/jas/skae260
102. Gunter SA, Beck PA, Phillips JK: Effects of supplementary selenium source on the performance and blood measurements in beef cows and their calves. J Anim Sci 2003;81:856-864. doi: 10.2527/2003.814856x
103. Aréchiga CF, Ortíz O, Hansen PJ: Effect of prepartum injection of vitamin E and selenium on postpartum reproductive function of dairy cattle. Theriogenology 1994;41:1251-1258. doi: 10.1016/0093-691x(94)90482-x
104. Ceko MJ, O’Leary S, Harris HH, et al: Trace elements in ovaries: measurement and physiology. Biol Reprod 2016;94:1-14. doi: 10.1095/biolreprod.115.137240
105.Abdel-Halim BR, Helmy NA: Effect of nano-selenium and nano-zinc particles during in vitro maturation on the developmental competence of bovine oocytes. Anim Prod Sci 2017;58:2021-2028. doi: 10.1071/AN17057
106.Xiong X, Lan D, Li J, Lin Y, Li M: Selenium supplementation during in vitro maturation enhances meiosis and developmental capacity of yak oocytes. Anim Sci J 2017;89:298-306. doi: 10.1111/asj.12894
107.Jeong YW, Hossein MS, Bhandari DP, et al: Effects of insulin–transferrin–selenium in defined and porcine follicular fluid supplemented IVM media on porcine IVF and SCNT embryo production. Anim Reprod Sci 2008;106:13-24. doi: 10.1016/j.anireprosci.2007.03.021
108. Rodriguez MD, Cittadini CO, Teplitz GM, et al: Canine IVM with SOF medium, insulin–transferrin–selenium, and low O2 tension improves oocyte meiotic competence and decreases reactive oxygen species levels. Front Cell Dev Biol 2021;9:694889. doi: 10.3389/fcell.2021.694889
109. Adeniran SO, Zheng P, Feng R, et al: The antioxidant role of selenium via GPx1 and GPx4 in LPS-induced oxidative stress in bovine endometrial cells. Biol Trace Elem Res 2022;200:1140-1155. doi: 10.1007/s12011-021-02731-0
110. Crites BR: The effects of form of selenium on the bovine corpus luteum, uterine endometrium, and development of the conceptus. Ph.D. Dissertation. Lexington, KY; University of Kentucky: 2021.
111. Borowicz P, Ward N, Caton J, et al: Effects of supernutritional levels of Selenium (Se) on vascular density and cell proliferation in the sheep placenta. J Anim Sci 2005;83:104.
112.Murphy VE, Smith R, Giles WB, et al: Endocrine regulation of human fetal growth: the role of the mother, placenta, and fetus. Endocr Rev 2006;27:141-169. doi: 10.1210/er.2005-0011
113.Nair S, Salomon C: Extracellular vesicles and their immunomodulatory functions in pregnancy. Semin Immunopathol 2018;5:425-437. doi: 10.1007/s00281-018-0680-2
114. Dahlen CR, Reynolds LP, Caton JS: Selenium supplementation and pregnancy outcomes. Front Nutr 2022;9:1011850. doi: 10.3389/fnut.2022.1011850
115. Mistry HD, Broughton Pipkin F, et al: Selenium in reproductive health. Am J Obstet Gynecol 2012;206:21-30. doi: 10.1016/j.ajog.2011.07.034
116.Mirone M, Giannetta E, Isidori AM: Selenium and reproductive function. A systematic review. J Endocrinol Invest 2013;36(10 Suppl):28-36.
117.Rayman MP, Wijnen H, Vader H, et al: Maternal selenium status during early gestation and risk for preterm birth. CMAJ 2011;183:549-555. doi: 10.1503/cmaj.101095
118. Mistry HD, Kurlak LO, Young SD, et al: Maternal selenium, copper and zinc concentrations in pregnancy associated with small-for-gestational-age infants. Matern Child Nutr 2014;10:327-334. doi: 10.1111/j.1740-8709.2012.00430.x
119. Parillo F, Sylla L, Palombi C, et al: Immunocytochemical localisation of phospholipid hydroperoxide glutathione peroxidase in bull’s spermatogenic cells. Ital J Anim Sci 2014;13:3483. doi: 10.4081/ijas.2014.3483
120. Rotruck JT, Pope AL, Ganther HE, et al: Selenium: biochemical role as a component of glutathione peroxidase. Science 1973;179:588-590. doi: 10.1126/science.179.4073.588
121. Sławeta R, Laskowska T, Szymańska E: Lipid peroxides, spermatozoa quality and activity of glutathione peroxidase in bull semen. Acta Physiol Pol 1988;39:207-214.
122. Bollwein H, Bittner L: Impacts of oxidative stress on bovine sperm function and subsequent in vitro embryo development. Anim Reprod 2018;15(Suppl 1):703-710. doi: 10.21451/1984-3143-AR2018-0041
123. Madeja ZE, Podralska M, Nadel A, et al: Mitochondria content and activity are crucial parameters for bull sperm quality evaluation. Antioxidants (Basel) 2021;10:1204. doi: 10.3390/antiox10081204
124. Pratt WD, Murray FA, Conrad HR, et al: Effects of selenium supplementation on bull sperm metabolism in vitro. Theriogenology 1980;13:369-379. doi: 10.1016/0093-691x(80)90049-7
125. Khalil WA, El-Harairy MA, Zeidan AEB, et al: Impact of selenium nano-particles in semen extender on bull sperm quality after cryopreservation. Theriogenology 2019;126:121-127. doi: 10.1016/j.theriogenology.2018.12.017
126. Sławeta R, Laskowska T, Szymańska E: Seasonal changes in total and selenium-dependent glutathione peroxidase activity in bovine semen in relation to lipid peroxide. Anim Reprod Sci 1988;17:303-307. doi: 10.1016/0378-4320(88)90067-X
127. Dorostkar K, Alavi-Shoushtari SM, Mokarizadeh A: Effects of in vitro selenium addition to the semen extender on the spermatozoa characteristics before and after freezing in water buffaloes (Bubalus bubalis). Vet Res Forum 2012;3:263-268.
128. Kasimanickam R, Kasimanickam V, Thatcher CD, et al: Relationships among lipid peroxidation, glutathione peroxidase, superoxide dismutase, sperm parameters, and competitive index in dairy bulls. Theriogenology 2007;67:1004-1012. doi: 10.1016/j.theriogenology.2006.11.013
129. Vinayamohan PG, Joseph D, Viju, LS, et al: Efficacy of selenium for controlling infectious diseases. In: Gelen V, Kara A, Kükürt A: editors. Selenium and Human Health. Rijeka, Croatia; IntechOpen: 2023. doi: 10.5772/intechopen.105312
130. Asadpour R, Aliyoldashi MH, Saberivand A, et al: Ameliorative effect of selenium nanoparticles on the structure and function of testis and in vitro embryo development in Aflatoxin B1-exposed male mice. Andrologia 2020;52:e13824. doi: 10.1111/and.13824
131. Hozyen HF, Khalil HMA, Ghandour RA, et al: Nano selenium protects against deltamethrin-induced reproductive toxicity in male rats. Toxicol Appl Pharmacol 2020;408:115274. doi: 10.1016/j.taap.2020.115274
132. Shi LG, Yang RJ, Yue WB, et al: Effect of elemental nano-selenium on semen quality, glutathione peroxidase activity, and testis ultrastructure in male Boer goats. Anim Reprod Sci 2010;118:248-254. doi: 10.1016/j.anireprosci.2009.10.003
133. Abd-Allah S, Hashem KS: Selenium nanoparticles increase the testicular antioxidant activity and spermatogenesis in male rats as compared to ordinary selenium. Int J Adv Res 2015;3:792-802
134. Toh P, Nicholson JL, Vetter AM, et al: Selenium in bodily homeostasis: hypothalamus, hormones, and highways of communication. Int J Mol Sci 2022;23:15445. doi: 10.3390/ijms232315445
135. Behne D, Weiler H, Kyriakopoulos A: Effects of selenium deficiency on testicular morphology and function in rats. J Reprod Fertil 1996;106:291-297. doi: 10.1530/jrf.0.1060291
136. Shi L, Song R, Yao X, et al: Effects of selenium on the proliferation, apoptosis and testosterone production of sheep Leydig cells in vitro. Theriogenology 2017;93:24-32. doi: 10.1016/j.theriogenology.2017.01.022
137. Shi L, Yue W, Zhang C, et al: Effects of maternal and dietary selenium (Se-enriched yeast) on oxidative status in testis and apoptosis of germ cells during spermatogenesis of their offspring in goats. Anim Reprod Sci 2010;119:212-218. doi: 10.1016/j.anireprosci.2010.02.012
138. Saaranen M, Suistomaa U, Kantola M, et al: Selenium in reproductive organs, seminal fluid and serum of men and bulls. Hum Reprod 1986;1:61-64. doi: 10.1093/oxfordjournals.humrep.a136361
139. Anchordoquy JP, Anchordoquy JM, Lizarraga RM, et al: The importance of trace minerals copper, manganese, selenium and zinc in bovine sperm–zona pellucida binding. Zygote 2019;27:89-96. doi: 10.1017/S0967199419000078
140. Swecker WS Jr, Eversole DE, Thatcher CD, et al: Influence of supplemental selenium on humoral immune responses in weaned beef calves. Am J Vet Res 1989;50:1760-1763.
141. Underwood WJ, Blauwiekel R, Delano ML, et al: Biology and diseases of ruminants (Sheep, Goats, and Cattle). In: Fox JG, Anderson LC, Otto GM, et al: editors. American College of Laboratory Animal Medicine, Laboratory Animal Medicine. 3rd edition, Academic Press: 2015. p. 623-694. doi: 10.1016/B978-0-12-409527-4.00015-8
142. Harsch JA: Clinical experiences with white muscle disease. AABP Conference Proceedings 1976; pp 70-71. doi: 10.21423/aabppro19767674
143. Buergelt CD, Sisk D, Chenoweth, PJ, et al: Nutritional myodegeneration associated with dorsal scapular displacement in beef heifers. J Comp Pathol 1996;114:445450. doi: 10.1016/s0021-9975(96)80019-3
144. Jia Y, Li Q, Burris WR, et al: Forms of selenium in vitamin-mineral mixes differentially affect serum prolactin concentration and hepatic glutamine synthetase activity of steers grazing endophyte-infected tall fescue. J Anim Sci 2018;96:715-727. doi: 10.1093/jas/skx068
145.Li Q, Jia Y, Burris WR, et al: Forms of selenium in vitamin-mineral mixes differentially affect the expression of genes responsible for prolactin, ACTH, and α-MSH synthesis and mitochondrial dysfunction in pituitaries of steers grazing endophyte-infected tall fescue. J Anim Sci 2019;97:631-643. doi: 10.1093/jas/sky438
146.Fox SR, Jong MT, Casanova J, et al: The homeodomain protein, Pit-1/GHF-1, is capable of binding to and activating cell-specific elements of both the growth hormone and prolactin gene promoters. Mol Endocrinol 1990;4:1069-1080. doi: 10.1210/mend-4-7-1069
147.Castaño A, Ayala A, Rodriguez-Gomez JA, et al: Increase in dopamine turnover and tyrosine hydroxylase enzyme in hippocampus of rats fed on low selenium diet. J Neurosci Res 1995;42:684-691. doi: 10.1002/jnr.490420511
148.Castaño A, Ayala A, Rodríguez-Gómez JA, et al: Low selenium diet increases the dopamine turnover in prefrontal cortex of the rat. Neurochem Int 1997;30:549-555. doi: 10.1016/s0197-0186(96)00123-4
149. Castaño A, Cano J, Machado A: Low selenium diet affects monoamine turnover differentially in substantia nigra and striatum. J Neurochem 1993;61:1302-1307. doi: 10.1111/j.1471-4159.1993.tb13622.x
150. Erskine RJ, Bartlett PC, Herdt T, et al: Effects of parenteral administration of vitamin E on health of periparturient dairy cows. J Am Vet Med Assoc 1997;211:466-469.
151. Seshadri P, Sisk D, Bowman F, et al: Leachability of Arsenic and Selenium in Submicron Coal Fly Ash. In Proceedings of the World of Coal Ash Conference, University of Kentucky and American Coal Ash Association, Denver, CO, USA, 9–12 May 2011.
152. National Research Council. National Research Council/1980: Issues and Current Studies. Washington, DC: The National Academies Press: 1981. doi: 10.17226/27527
153. Rosenfeld I, Beath OA: The influence of protein diets on selenium poisoning. Am J Vet Res 1946;7:52-56.
154. Rosenfeld I, Beath OA: The influence of various substances on chronic selenium poisoning. J Pharmacol Exp Ther 1947;91:218-223. doi: 10.1016/S0022-3565(25)03098-8
155. Maag, DD, Glenn MW: Toxicity of selenium: farm animals. In Muth OA: editor. Selenium in Biomedicine: A Symposium. Westport, CT; AVI Publishing Co: 1967. p. 127-140.
156. Panter KE, Ralphs MH, Pfister JA, et al: Plants Poisonous to Livestock in the Western States. U.S. Department of Agriculture, Agriculture Bulletin No. 415. 2011. p. 45-46 and p. 105-107.
157. Combs GF Jr, Combs SB: The Role of Selenium in Nutrition. San Diego, CA; Academic Press: 1986. p. 413-462.
158. Basini G, Tamanini C: Selenium stimulates estradiol production in bovine granulosa cells: possible involvement of nitric oxide. Domest Anim Endocrinol 2000;18:1-17. doi: 10.1016/s0739-7240(99)00059-4
159. Yaeger MJ, Neiger RD, Holler L, et al: The effect of subclinical selenium toxicosis on pregnant beef cattle. J Vet Diagn Invest 1998;10:268-273. doi: 10.1177/104063879801000307
160. Abutarbush SM, Radostits OM: Congenital nutritional muscular dystrophy in a beef calf. Can Vet J 2003;44:738-739. PMC340271
161. Draize JH, Beath OA: Observations on the pathology of blind staggers and alkali disease. J Am Vet Med Assoc 1935;86:753-763.
162. 3 Health effects. In: Toxicological Profile for Selenium. Atlanta, GA; Agency for Toxic Substances and Disease Registry (US): 2003. Available from: https://www.ncbi.nlm.nih.gov/books/NBK600364/ [cited 10 January 2025].
163. Miksa IR, Buckley CL, Carpenter NP, et al: Comparison of selenium determination in liver samples by atomic absorption spectroscopy and inductively coupled plasma-mass spectrometry. J Vet Diagn Invest 2005;17:331-340. doi: 10.1177/104063870501700405
164. National Research Council (US) Subcommittee on Selenium. 7 effects of excess selenium. In: Selenium in Nutrition: Revised Edition. Washington, DC; National Academies Press (US): 1983. Available from: https://www.ncbi.nlm.nih.gov/books/NBK216723/ [cited 10 January 2025].
165. Nuttall KL: Evaluating selenium poisoning. Ann Clin Lab Sci 2006;36:409-420. PMID: 17127727
166. Davis TZ, Stegelmeier BL, Panter KE, et al: Toxicokinetics and pathology of plant-associated acute selenium toxicosis in steers. J Vet Diagn Invest 2012;24:319-327. doi: 10.1177/1040638711435407
167. Toxicological Profile for Selenium. Atlanta, GA; Agency for Toxic Substances and Disease Registry (US): 2003. Available from: https://www.ncbi.nlm.nih.gov/books/NBK600367/ [cited 10 January 2025].
168. Brummer FA, Pirelli GJ, Hall JA: Selenium supplementation strategies for livestock in Oregon. EM 9094. 2014. p. 1-9. Available from: https://oregonsheepcommission.com/wp-content/uploads/Selenium-Supplementation-Strategies-for-Livestock-in-Oregon.pdf [cited 29 June 2023].
169. Swecker WS Jr, Thatcher CD, Eversole DE, et al: Effect of selenium supplementation on colostral IgG concentration in cows grazing selenium-deficient pastures and on postsuckle serum IgG concentration in their calves. Am J Vet Res 1995;56:450-453. PMID: 7785820
170. Selenium effects on South Dakota livestock production. Available from: https://danr.sd.gov/Agriculture/Inspection/FeedRemedy/docs/selenium-brochure.pdf [cited 10 January 2025].
171. Terry N, Zayed AM, De Souza MP, et al: Selenium in higher plants. Annu Rev Plant Physiol Plant Mol Biol 2000;51:401-432. doi: 10.1146/annurev.arplant.51.1.401