BACKGROUND: To protect from toxicity at supra-essential doses of selenium, it is important to determine dose levels at which adverse effects occur.
METHODS: We identified relevant literature on the repeated dosage of selenium and extracted dose descriptors on reported endpoints, except on genotoxicity/carcinogenicity.
RESULTS: Selenium forms with toxicological data were organic ones: selenomethionine, selenocystine/selenocysteine; and inorganic ones, including selenite (SeO32-), selenate (SeO42-), selenium sulphide (SeS2), selenide (Se2-) and selenium nanoparticles. Clinical signs of selenium toxicity in humans include a garlicky-smelling breath, hair loss, and nail changes. One human study showed increased mortality following daily ingestion of 300 µg Se per day for 5 years, equal to a lowest-observed-adverse-effect level (LOAEL) of ∼4.3 µg/kg bw/days. The corresponding no-observed-adverse-effect level (NOAEL) was ∼2.9 µg Se/kg bw/day. One study reported an increased risk of type 2 diabetes after ∼2.9 µg Se/kg bw/day, but other studies with similar doses found no increases in mortality or incidence of type 2 diabetes. NOAELs on affected body weight in animal studies were 0.24-1.2 mg Se/kg bw/day. Other endpoints of selenium toxicity in animals include hepatotoxicity with a NOAEL as low as 2 µg/kg bw/day in rats, as well as gastrointestinal, cardiovascular, and reproductive toxicities with NOAELs of 0.6 (gastrointestinal), 0.08, and 0.4 (cardiovascular) and ≥ 0.04 mg Se/kg bw/day (reproductive), respectively.
CONCLUSIONS: Dose descriptors describing selenium toxicity were as low as 2-3 µg Se/kg bw/day.

BACKGROUND: Selenium is a trace element traditionally ingested either in its organic form via food or in its inorganic form through nutritional supplements, while selenium formulated as nanoparticles is a putative long-acting alternative. To understand the physiology and toxicology of the different selenium formulations, it is important to determine how their selenium content is absorbed, distributed, metabolised and excreted; therefore, we reviewed their biokinetics following oral exposure.
METHODS: We retrieved and reviewed the literature on the absorption, distribution, metabolism, and excretion of oral exposure to different forms of selenium.
RESULTS: Selenium in both the organic form (containing carbon to selenium chemical bonds) and the inorganic form is absorbed into the blood in humans. The mean normal blood level of many studies was 139 μg/L. There are indications that selenium from organic sources is more bioavailable than selenium from inorganic sources. Selenium is distributed throughout the body, including in breast milk. The elimination of selenium mainly involves the faecal and urinary pathways, whereas breath, saliva and hair are minor contributors. Urinary metabolites include trimethylselenium ions, selenosugars and Se-methylselenoneine.
CONCLUSIONS: Selenium is absorbed to a high extent, and selenium from organic sources is more bioavailable than from inorganic sources. Selenium, as expected as an essential trace element, is distributed throughout the body. Selenium is extensively metabolised, and various excretion metabolites have been identified in both urine and breath, while some selenium is also excreted via faeces.

Exercise overproduces oxygen reactive species (ROS) and eventually exceeds the body\'s antioxidant capacity to neutralize them. The ROS produce damaging effects on the cell membrane and contribute to skeletal muscle damage. Selenium (Se), a natural mineral trace element, is an essential component of selenoproteins that plays an important role in antioxidant defense. The activity of the enzyme glutathione peroxidase (GPx), a highly-efficient antioxidant enzyme, is closely dependent on the presence of Se. These properties of Se may be potentially applicable to improve athletic performance and training recovery. We systematically searched for published studies to evaluate the effectiveness of Se supplementation on antioxidant defense system, muscle performance, hormone response, and athletic performance among physically active individuals. We used the Preferred Reporting Elements for Systematic Reviews and Meta-Analysis (PRISMA) guidelines and searched in SCOPUS, Web of Science (WOS), and PubMed databases to identify published studies until March 2020. The systematic review incorporated original studies with randomized controlled crossover or parallel design in which intake of Se administered once a day was compared with the same placebo conditions. No exclusions were applied for the type of physical exercise performed, the sex, nor the age of the participants. Among 150 articles identified in the search, 6 met the criteria and were included in the systematic review. The methodological quality of the studies was evaluated using the McMaster Critical Review Form. Oral Se supplementation with 180 µg/day or 240 µg/day (selenomethionine) and 200 µg/day (Sodium Selenite), significantly decreased lipid hydroperoxide levels and increased GPx in plasma, erythrocyte, and muscle. No significant effects were observed on athletic performance, testosterone hormone levels, creatine kinase activity, and exercise training-induced adaptations on oxidative enzyme activities or on muscle fiber type myosin heavy chain expression. In addition, Se supplementation showed to have a dampening effect on the mitochondria changes in chronic and acute exercise. In summary, the use of Se supplementation has no benefits on aerobic or anaerobic athletic performance but it may prevent Se deficiencies among athletes with high-intensity and high-volume training. Optimal Se plasma levels may be important to minimize chronic exercise-induced oxidative effects and modulate the exercise effect on mitochondrial changes.

HIV infection has been linked to selenium deficiency which, in turn, is thought to be associated with a high risk of tuberculosis and mortality in HIV-infected patients. Furthermore, several trials have reported the beneficial effects of selenium supplementation in patients with HIV. However, the evidence remains inconclusive. Our study aimed to investigate whether daily selenium supplementation in patients infected with HIV delays the progression of HIV infection.
A systematic review was performed using EMBASE and Medline databases from January 2000 to June 2018. We included randomized clinical trials in adults comparing selenium with placebo and reporting outcomes including its effect on HIV viral load and cluster of differentiation 4 cell count (CD4).
Six out of the 507 retrieved articles that met the inclusion criteria were used in this review. Reviewed studies show that daily supplementation with 200 μg selenium may improve the rate of cluster of differentiation 4 (CD4) count. The length of selenium supplementation and follow-up varied from 9 to 24 months. Supplements were well tolerated in all reviewed studies. Whether daily selenium supplementation in HIV-infected persons suppresses HIV-infection requires further investigation as existing data are heterogeneous.
We found some clinical evidence that selenium supplementation can delay CD4 decline in HIV-infected patients, thus prolonging the onset of AIDS. However, we did not find quantifiable evidence that selenium supplementation suppresses or reduces HIV viral load.

Similar to other tissues selenium from selenomethionine is deposited in the brain at higher concentrations than selenium in other forms. Vitamin E has a greater effect than selenium in reducing lipid peroxidation in various brain regions. Selenium does not have as great effect on glutathione peroxidase (GPX) activity in the brain as in most other organs. Prolonged selenium and iodine deficiencies will compromise thyroid hormone homeostatus in the brain and this is due to changes in deiodinases activities and lipid peroxidation. Even though selenium deficiency results in reduced GPX activity and selenium content in the brain, there is no reduction in thioredoxin reductase activity or selenoprotein W levels. Selenoprotein P is taken up in greater amounts by the brain but not by other organs in selenium deficient animals, suggesting a critical function of this selenoprotein in this organ. Selenium will influence compounds with hormonal activity (and neurotransmitters) in the brain, and this is postulated to be the reason selenium affects moods in humans and behavior in animals. Even though selenium counteracts the neurotoxicity of mercury, cadmium, lead and vanadium, it causes them to accumulate in the brain, presumably in a nontoxic complex.

Although the need for selenium in human and animal nutrition is well recognized, the question concerning the proper form of selenium for supplemental use is still being debated. Ideally, selenium should be supplemented in the form in which it occurs naturally in foods. Because the L-isomer of selenomethionine (Se-met) is a major natural food-form of selenium, synthetic L-Se-met or enriched food sources thereof such as selenium yeast are appropriate supplemental forms of Se for humans; for animals, DL-Se-met is acceptable. Ingested Se-met is either metabolized directly to reactive forms of selenium or stored in place of methionine in body proteins. Se-met metabolism is closely linked to protein turnover. At constant intakes in the nutritional range, tissue Se levels increase until a steady state is established, preventing the build-up to toxic levels.

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