Selenium in biology

Last updated

Selenocysteine is the main organic molecule involving selenium in humans. Selenocysteine skeletal 3D.svg
Selenocysteine is the main organic molecule involving selenium in humans.

Selenium is an essential micronutrient for animals, though it is toxic in large doses. In plants, it sometimes occurs in toxic amounts as forage, e.g. locoweed. Selenium is a component of the amino acids selenocysteine and selenomethionine. In humans, selenium is a trace element nutrient that functions as cofactor for glutathione peroxidases and certain forms of thioredoxin reductase. [1] Selenium-containing proteins are produced from inorganic selenium via the intermediacy of selenophosphate (PSeO33−).

Contents

Se-containing biomolecules

Selenium is an essential micronutrient in mammals, but is also recognized as toxic in excess. Selenium exerts its biological functions through selenoproteins, which contain the amino acid selenocysteine. Twenty-five selenoproteins are encoded in the human genome. [2]

Glutathione peroxidase

The glutathione peroxidase family of enzymes (abbreviated GSH-Px) catalyze reduction of hydrogen peroxide and organic hydroperoxides:

2GSH + H2O2 → GSSG + 2 H2O

The two H atoms are donated by thiols in a process that begins with oxidation of a selenol side chain in GSH-Px. The organoselenium compound ebselen is a drug used to supplement the action of GSH-Px. It functions as a catalyst for the destruction of hydrogen peroxide. [3]

A related selenium-containing enzyme in some plants and in animals (thioredoxin reductase) generates reduced thioredoxin, a dithiol that serves as an electron source for peroxidases and also the important reducing enzyme ribonucleotide reductase that makes DNA precursors from RNA precursors. [4]

Deiodinases

Selenium also plays a role in the functioning of the thyroid gland. It participates as a cofactor for the three thyroid hormone deiodinases. These enzymes activate and then deactivate various thyroid hormones and their metabolites. [5] It may inhibit Hashimoto's disease, an auto-immune disease in which the body's own thyroid cells are attacked by the immune system. A reduction of 21% on TPO antibodies was reported with the dietary intake of 0.2 mg of selenium. [6]

Formate dehydrogenase

Some microorganisms utilize selenium in formate dehydrogenase. Formate is produced in large amounts in the hepatic (liver cells) mitochondria of embryonic cells and in cancer cells by the folate cycle. [7]

Formate is reversibly oxidized by the enzyme formate dehydrogenase: [8]

HCO2− → CO2 + H+ + 2 e−

Thioredoxin reductase

Thioredoxin reductase uses a cysteine-selenocysteine pair to reduce the disulfide in thioredoxin. The selenocysteine is arranged in an unusual Sec-His-Glu catalytic triad, which tunes its pKa. [9]

Indicator plants

Certain species of plants are considered indicators of high selenium content of the soil, since they require high levels of selenium to thrive. The main selenium indicator plants are Astragalus species (including some locoweeds), prince's plume ( Stanleya sp.), woody asters ( Xylorhiza sp.), and false goldenweed ( Oonopsis sp.) [10]

Medical use of synthetic selenium compounds

The substance loosely called selenium sulfide (with the approximate formula SeS2) is the active ingredient in some anti-dandruff shampoos. [11] The selenium compound kills the scalp fungus Malassezia , which causes shedding of dry skin fragments. The ingredient is also used in body lotions to treat Tinea versicolor due to infection by a different species of Malassezia fungus. [12]

Several clinical trials have assessed the use of selenium supplements in critically ill adults; however, the effectiveness and potential benefits of selenium supplementation in this context is not well understood. [13]

Detection in biological fluids

Selenium may be measured in blood, plasma, serum or urine to monitor excessive environmental or occupational exposure, confirm a diagnosis of poisoning in hospitalized victims or to assist in a forensic investigation in a case of fatal overdosage. Some analytical techniques are capable of distinguishing organic from inorganic forms of the element. Both organic and inorganic forms of selenium are largely converted to monosaccharide conjugates (selenosugars) in the body prior to being eliminated in the urine. Cancer patients receiving daily oral doses of selenothionine may achieve very high plasma and urine selenium concentrations. [14]

Toxicity

Although selenium is an essential trace element, it is toxic if taken in excess. Exceeding the Tolerable Upper Intake Level of 400 micrograms per day can lead to selenosis. [15] This 400 microgram (μg) Tolerable Upper Intake Level is based primarily on a 1986 study of five Chinese patients who exhibited overt signs of selenosis and a follow-up study on the same five people in 1992. [16] The 1992 study actually found the maximum safe dietary Se intake to be approximately 800 micrograms per day (15 micrograms per kilogram body weight), but suggested 400 micrograms per day to not only avoid toxicity, but also to avoid creating an imbalance of nutrients in the diet and to account for data from other countries. [17] In China, people who ingested corn grown in extremely selenium-rich stony coal (carbonaceous shale) have suffered from selenium toxicity. This coal was shown to have selenium content as high as 9.1%, the highest concentration in coal ever recorded in literature. [18]

Symptoms of selenosis include a garlic odor on the breath, gastrointestinal disorders, hair loss, sloughing of nails, fatigue, irritability, and neurological damage. Extreme cases of selenosis can result in cirrhosis of the liver, pulmonary edema, and death. [19] Elemental selenium and most metallic selenides have relatively low toxicities because of their low bioavailability. By contrast, selenates and selenites are very toxic, having an oxidant mode of action similar to that of arsenic trioxide. The chronic toxic dose of selenite for humans is about 2400 to 3000 micrograms of selenium per day for a long time. [20] Hydrogen selenide is an extremely toxic, corrosive gas. [21] Selenium also occurs in organic compounds, such as dimethyl selenide, selenomethionine, selenocysteine and methylselenocysteine, all of which have high bioavailability and are toxic in large doses.

Selenium poisoning of water systems may result whenever new agricultural runoff courses through normally dry, undeveloped lands. This process leaches natural soluble selenium compounds (such as selenates) into the water, which may then be concentrated in new "wetlands" as the water evaporates. High selenium levels produced in this fashion have been found to have caused certain congenital disorders in wetland birds. [22]

Relationship between survival of juvenile salmon and concentration of selenium in their tissues after 90 days (Chinook salmon: Hamilton et al. 1990) or 45 days (Atlantic salmon: Poston et al. 1976) exposure to dietary selenium. The 10% lethality level (LC10=1.84 mg/g) was derived by applying the biphasic model of Brain and Cousens (1989) to only the Chinook salmon data. The Chinook salmon data comprise two series of dietary treatments, combined here because the effects on survival are indistinguishable. Se dose-response curve for juvenile salmon mortality - percent scale.jpg
Relationship between survival of juvenile salmon and concentration of selenium in their tissues after 90 days (Chinook salmon: Hamilton et al. 1990) or 45 days (Atlantic salmon: Poston et al. 1976) exposure to dietary selenium. The 10% lethality level (LC10=1.84 μg/g) was derived by applying the biphasic model of Brain and Cousens (1989) to only the Chinook salmon data. The Chinook salmon data comprise two series of dietary treatments, combined here because the effects on survival are indistinguishable.

In fish and other wildlife, low levels of selenium cause deficiency while high levels cause toxicity. For example, in salmon, the optimal concentration of selenium in the fish tissue (whole body) is about 1 microgram selenium per gram of tissue (dry weight). At levels much below that concentration, young salmon die from selenium deficiency; [23] much above that level they die from toxic excess. [24]

Deficiency

Selenium deficiency can occur in patients with severely compromised intestinal function, those undergoing total parenteral nutrition, and [25] in those of advanced age (over 90). Also, people dependent on food grown from selenium-deficient soil are at risk. Although New Zealand has low levels of selenium in its soil, adverse health effects have not been detected. [26]

Selenium deficiency as defined by low (<60% of normal) selenoenzyme activity levels in brain and endocrine tissues only occurs when a low selenium status is linked with an additional stress, such as high exposures to mercury [27] or as a result of increased oxidant stress due to vitamin E deficiency. [28]

Selenium interacts with other nutrients, such as iodide and vitamin E. The interaction is observed in the etiology of many deficiency diseases in animals, and pure selenium deficiency is rare. The effect of selenium deficiency on health remains uncertain, particularly in relation to Kashin-Beck disease. [29]

Dietary recommendations

The US Institute of Medicine (IOM) updated Estimated Average Requirements (EARs) and Recommended Dietary Allowances (RDAs) for selenium in 2000. If there is not sufficient information to establish EARs and RDAs, an estimate designated Adequate Intake (AI) is used instead. The current EAR for selenium for people ages 14 and up is 45 μg/day. The RDA is 55 μg/day. RDAs are higher than EARs so as to identify amounts that will cover people with higher-than-average requirements. RDA for pregnancy is 60 μg/day. RDA for lactation is 70 μg/day. For children ages 1–13 years, the RDA increases with age from 20 to 40 μg/day. As for safety, the IOM sets Tolerable upper intake levels (ULs) for vitamins and minerals when evidence is sufficient. In the case of selenium, the UL is 400 μg/day. Collectively the EARs, RDAs, AIs and ULs are referred to as Dietary Reference Intakes (DRIs). [30]

The European Food Safety Authority (EFSA) refers to the collective set of information as Dietary Reference Values, with Population Reference Intake (PRI) instead of RDA, and Average Requirement instead of EAR. AI and UL are defined the same as in the United States. For women and men ages 15 and older, the AI is set at 70 μg/day. AI for pregnancy is 70 μg/day; for lactation, 85 μg/day. For children ages 1–14 years, the AIs increase with age from 15 to 55 μg/day. These AIs are higher than the U.S. RDAs. [31] The European Food Safety Authority reviewed the same safety question and set its UL at 300 μg/day, which is lower than the U.S. value. [32]

In the United States, selenium deficiency is not common. A federal survey of food consumption determined that for women and men over the age of 19, average consumption from foods and beverages was 89 and 125 μg/day, respectively. For women and men of all ages fewer than 3% consumed less than the EAR. [33]

Labeling

For US food and dietary supplement labeling purposes, the amount in a serving is expressed as a percent of Daily Value (%DV). For selenium labeling purposes, 100% of the Daily Value was 70 μg, but as of 27 May 2016 it was revised to 55 μg. [34] [35] A table of the old and new adult daily values is provided at Reference Daily Intake.

Food sources

Dietary selenium comes from nuts, cereals, meat, mushrooms, fish, and eggs. Brazil nuts are the richest ordinary dietary source and could cause selenium toxicity if consumed regularly – though the actual concentration of selenium (as with any plant-based food sources, such as another selenium-accumulating "paradise nut" Lecythis, belonging to the same family Lecythidaceae) is soil-dependent and may vary significantly by geographic location. In descending order of concentration, high levels are also found in kidney, tuna, crab, and lobster. [36] [37]

The human body's content of selenium is believed to be in the 13–20 milligram range. [38]

Human health

Selenium in cancer

Selenium at nutritional levels is required for cell homeostasis, playing a role as an anti-oxidant through selenoproteins, thus, act chemo-preventive against cancer. In contrast, supra-nutritional levels act as pro-oxidant toxic in tumour cells. Selenium paradox.jpg
Selenium at nutritional levels is required for cell homeostasis, playing a role as an anti-oxidant through selenoproteins, thus, act chemo-preventive against cancer. In contrast, supra-nutritional levels act as pro-oxidant toxic in tumour cells.

Selenium has bimodal biological action depending on the concentration. At low nutritional doses, selenium acts as an antioxidant through selenoproteins, scavenging ROS, supporting cell survival and growth; while, at supra-nutritional higher pharmacological doses, selenium acts as a pro-oxidant generating ROS and inducing cell death. In cancer, studies have been conducted mostly on the benefits of selenium intake in reducing the risk of cancer incidence at the nutritional level; however, fewer studies have explored the effects of supra-nutritional or pharmacological doses of selenium on cancer. [39]

"Although an inverse association between selenium exposure and the risk of some types of cancer was found in some observational studies, this cannot be taken as evidence of a causal relation, and these results should be interpreted with caution... Conflicting results including inverse, null and direct associations have been reported for some cancer types... RCTs assessing the effects of selenium supplementation on cancer risk have yielded inconsistent results... To date, no convincing evidence suggests that selenium supplements can prevent cancer in humans." [40]

Selenium in anti-tumour immunity

To date, many studies have been conducted on the benefits of selenium intake in reducing the risk of cancer incidence at the nutritional level, indicating that likely selenium functions as an immunostimulator, i.e. reversing the immunosuppression in tumour microenvironment towards antitumour immunity by activating immune cells (e.g. M1 macrophages and CD8+ T-lymphocytes, the elevated number of neutrophils and activated cytotoxic NK cells) and releasing pro-inflammatory cytokines such as IFNγ and TNFα. [39]

Selenium can either play a pro-oxidant role inducing ROS, activating the Akt-NF-kB pathway or play an antioxidant role through selenoprotein synthesis such as TXNRD relocating to the nucleus and activating NF-kB, resulting in further activation of leukocytes and pro-inflammatory cytokine genes. Selenium and anti-tumour immunity.jpg
Selenium can either play a pro-oxidant role inducing ROS, activating the Akt–NF–кB pathway or play an antioxidant role through selenoprotein synthesis such as TXNRD relocating to the nucleus and activating NF-кB, resulting in further activation of leukocytes and pro-inflammatory cytokine genes.

HIV/AIDS

AIDS appears to involve a slow and progressive decline in levels of selenium in the body. Whether this decline in selenium levels is a direct result of the replication of HIV or related more generally to the overall malabsorption of nutrients by AIDS patients remains debated. Observational studies have found an association between decreased selenium levels and poorer outcomes in patients with HIV, though these studies were mostly done prior to the currently effective treatments with highly active antiretroviral therapy (HAART). Currently there is inadequate evidence to recommend routine selenium supplementation for HIV patients, and further research is recommended. [41]

Mortality

Selenium supplementation has no effect on overall mortality. [42]

Tuberculosis

As with other types of supplementation, there is no good evidence selenium supplementation helps in the treatment of tuberculosis. [43]

Diabetes

A meta-analysis of four RCTs concluded that there is no support for selenium supplementation for prevention of type 2 diabetes mellitus in Caucasians. [44]

Human reproductive system

Abnormally high or low levels of dietary selenium can have an adverse effect on sperm quality, with a consequent lowering of fertility. [45]

COVID-19

During the COVID-19 pandemic, some studies attempted to establish a correlation between selenium plasma level and severity of COVID-19 cases. One study done on 33 patients concluded that low plasma selenium levels were correlated with a high mortality rate among COVID-19 patients. However, the median age of deaths in this study was 89 years old; in contrast, survivors' median age was 69 years old, and the study stated that the causality remains unknown. [46] On the other hand, another study revealed that the mean selenium plasma level was within the normal range among all included COVID-19 patients; however, the mean selenium plasma level was elevated among severe cases of COVID-19. This study concluded that there was a significant elevation of selenium serum level among severe cases compared to non-severe cases of COVID-19, and could be correlated with the disease severity. [47]

Mercury poisoning

Selenium has a protective effect towards mercury toxicity. Mercury binds to selenium with high affinity, so this metal can inhibit selenium-dependent enzymes. However, increased selenium intake can preserve the enzyme activities, reducing the adverse effects caused by mercury exposure. [48] [49]

Evolution in biology and biosynthetic considerations

Selenium is incorporated into several prokaryotic selenoprotein families in bacteria, archaea, and eukaryotes as selenocysteine, [50] where selenoprotein peroxiredoxins protect bacterial and eukaryotic cells against oxidative damage. Selenoprotein families of GSH-Px and the deiodinases of eukaryotic cells seem to have a bacterial phylogenetic origin. The selenocysteine-containing form occurs in species as diverse as green algae, diatoms, sea urchin, fish and chicken. Selenium enzymes are involved in utilization of the small reducing molecules glutathione and thioredoxin.

Trace elements involved in GSH-Px and superoxide dismutase enzymes activities, i.e. selenium, vanadium, magnesium, copper, and zinc, may have been lacking in some terrestrial mineral-deficient areas. [50] Marine organisms retained and sometimes expanded their seleno-proteomes, whereas the seleno-proteomes of some terrestrial organisms were reduced or completely lost. These findings suggest that aquatic life supports selenium utilization, whereas terrestrial habitats lead to reduced use of this trace element. [51] [52] Marine fishes and vertebrate thyroid glands have the highest concentration of selenium and iodine. From about 500 Mya, freshwater and terrestrial plants slowly optimized the production of "new" endogenous antioxidants such as ascorbic acid (Vitamin C), polyphenols (including flavonoids), tocopherols, etc. A few of these appeared more recently, in the last 50–200 million years, in fruits and flowers of angiosperm plants. In fact, the angiosperms (the dominant type of plant today) and most of their antioxidant pigments evolved during the late Jurassic period.

About 200 Mya, new selenoproteins were developed as mammalian GSH-Px enzymes. [53] [54] [55] [56]

See also

Related Research Articles

Antioxidants are compounds that inhibit oxidation, a chemical reaction that can produce free radicals. Autoxidation leads to degradation of organic compounds, including living matter. Antioxidants are frequently added to industrial products, such as polymers, fuels, and lubricants, to extend their usable lifetimes. Foods are also treated with antioxidants to forestall spoilage, in particular the rancidification of oils and fats. In cells, antioxidants such as glutathione, mycothiol, or bacillithiol, and enzyme systems like superoxide dismutase, can prevent damage from oxidative stress.

<span class="mw-page-title-main">Riboflavin</span> Vitamin, dietary supplement, and yellow food dye

Riboflavin, also known as vitamin B2, is a vitamin found in food and sold as a dietary supplement. It is essential to the formation of two major coenzymes, flavin mononucleotide and flavin adenine dinucleotide. These coenzymes are involved in energy metabolism, cellular respiration, and antibody production, as well as normal growth and development. The coenzymes are also required for the metabolism of niacin, vitamin B6, and folate. Riboflavin is prescribed to treat corneal thinning, and taken orally, may reduce the incidence of migraine headaches in adults.

<span class="mw-page-title-main">Selenium</span> Chemical element with atomic number 34 (Se)

Selenium is a chemical element; it has the symbol Se and atomic number 34. It is a nonmetal with properties that are intermediate between the elements above and below in the periodic table, sulfur and tellurium, and also has similarities to arsenic. It seldom occurs in its elemental state or as pure ore compounds in Earth's crust. Selenium was discovered in 1817 by Jöns Jacob Berzelius, who noted the similarity of the new element to the previously discovered tellurium.

<span class="mw-page-title-main">Vitamin C</span> Essential nutrient found in citrus fruits and other foods

Vitamin C is a water-soluble vitamin found in citrus and other fruits, berries and vegetables. It is also a generic prescription medication and in some countries is sold as a non-prescription dietary supplement. As a therapy, it is used to prevent and treat scurvy, a disease caused by vitamin C deficiency.

Vitamin E is a group of eight fat soluble compounds that include four tocopherols and four tocotrienols. Vitamin E deficiency, which is rare and usually due to an underlying problem with digesting dietary fat rather than from a diet low in vitamin E, can cause nerve problems. Vitamin E is a fat-soluble antioxidant which may help protect cell membranes from reactive oxygen species. Worldwide, government organizations recommend adults consume in the range of 3 to 15 mg per day. As of 2016, consumption was below recommendations according to a worldwide summary of more than one hundred studies that reported a median dietary intake of 6.2 mg per day for alpha-tocopherol. Foods rich in vitamin E include seeds and nuts, seed oils, peanut butter, and vitamin E-fortified foods, such as margarine.

Vitamin B<sub>6</sub> Class of chemically related vitamins

Vitamin B6 is one of the B vitamins, and thus an essential nutrient. The term refers to a group of six chemically similar compounds, i.e., "vitamers", which can be interconverted in biological systems. Its active form, pyridoxal 5′-phosphate, serves as a coenzyme in more than 140 enzyme reactions in amino acid, glucose, and lipid metabolism.

<span class="mw-page-title-main">Vitamin A</span> Essential nutrient

Vitamin A is a fat-soluble vitamin, hence an essential nutrient. The term "vitamin A" encompasses a group of chemically related organic compounds that includes retinol, retinal, retinoic acid, and several provitamin (precursor) carotenoids, most notably beta-carotene. Vitamin A has multiple functions: essential in embryo development for growth, maintaining the immune system, and healthy vision, where it combines with the protein opsin to form rhodopsin – the light-absorbing molecule necessary for both low-light and color vision.

<span class="mw-page-title-main">Retinol</span> Chemical compound

Retinol, also called vitamin A1, is a fat-soluble vitamin in the vitamin A family that is found in food and used as a dietary supplement. Retinol or other forms of vitamin A are needed for vision, cellular development, maintenance of skin and mucous membranes, immune function and reproductive development. Dietary sources include fish, dairy products, and meat. As a supplement it is used to treat and prevent vitamin A deficiency, especially that which results in xerophthalmia. It is taken by mouth or by injection into a muscle. As an ingredient in skin-care products, it is used to reduce wrinkles and other effects of skin aging.

<span class="mw-page-title-main">Folate</span> Vitamin B9; nutrient essential for DNA synthesis

Folate, also known as vitamin B9 and folacin, is one of the B vitamins. Manufactured folic acid, which is converted into folate by the body, is used as a dietary supplement and in food fortification as it is more stable during processing and storage. Folate is required for the body to make DNA and RNA and metabolise amino acids necessary for cell division and maturation of blood cells. As the human body cannot make folate, it is required in the diet, making it an essential nutrient. It occurs naturally in many foods. The recommended adult daily intake of folate in the U.S. is 400 micrograms from foods or dietary supplements.

A nutrient is a substance used by an organism to survive, grow and reproduce. The requirement for dietary nutrient intake applies to animals, plants, fungi and protists. Nutrients can be incorporated into cells for metabolic purposes or excreted by cells to create non-cellular structures such as hair, scales, feathers, or exoskeletons. Some nutrients can be metabolically converted into smaller molecules in the process of releasing energy such as for carbohydrates, lipids, proteins and fermentation products leading to end-products of water and carbon dioxide. All organisms require water. Essential nutrients for animals are the energy sources, some of the amino acids that are combined to create proteins, a subset of fatty acids, vitamins and certain minerals. Plants require more diverse minerals absorbed through roots, plus carbon dioxide and oxygen absorbed through leaves. Fungi live on dead or living organic matter and meet nutrient needs from their host.

Vitamin deficiency is the condition of a long-term lack of a vitamin. When caused by not enough vitamin intake it is classified as a primary deficiency, whereas when due to an underlying disorder such as malabsorption it is called a secondary deficiency. An underlying disorder can have 2 main causes:

<span class="mw-page-title-main">Glutathione peroxidase</span> Enzyme family protecting the organism from oxidative damages

Glutathione peroxidase (GPx) is the general name of an enzyme family with peroxidase activity whose main biological role is to protect the organism from oxidative damage. The biochemical function of glutathione peroxidase is to reduce lipid hydroperoxides to their corresponding alcohols and to reduce free hydrogen peroxide to water.

In molecular biology a selenoprotein is any protein that includes a selenocysteine amino acid residue. Among functionally characterized selenoproteins are five glutathione peroxidases (GPX) and three thioredoxin reductases, (TrxR/TXNRD) which both contain only one Sec. Selenoprotein P is the most common selenoprotein found in the plasma. It is unusual because in humans it contains 10 Sec residues, which are split into two domains, a longer N-terminal domain that contains 1 Sec, and a shorter C-terminal domain that contains 9 Sec. The longer N-terminal domain is likely an enzymatic domain, and the shorter C-terminal domain is likely a means of safely transporting the very reactive selenium atom throughout the body.

β-Carotene Red-orange pigment of the terpenoids class

β-Carotene (beta-carotene) is an organic, strongly colored red-orange pigment abundant in fungi, plants, and fruits. It is a member of the carotenes, which are terpenoids (isoprenoids), synthesized biochemically from eight isoprene units and thus having 40 carbons.

<span class="mw-page-title-main">Vitamin D toxicity</span> Human disease

Vitamin D toxicity, or hypervitaminosis D is the toxic state of an excess of vitamin D. The normal range for blood concentration in adults is 20 to 50 nanograms per milliliter (ng/mL).

Chromium deficiency is described as the consequence of an insufficient dietary intake of the mineral chromium. Chromium was first proposed as an essential element for normal glucose metabolism in 1959, but its biological function has not been identified. Cases of deficiency were described in people who received all of their nutrition intravenously for long periods of time.

Vitamin B<sub><small>12</small></sub> Vitamin used in animal cells metabolism

Vitamin B12, also known as cobalamin, is a water-soluble vitamin involved in metabolism. It is one of eight B vitamins. It is required by animals, which use it as a cofactor in DNA synthesis, and in both fatty acid and amino acid metabolism. It is important in the normal functioning of the nervous system via its role in the synthesis of myelin, and in the circulatory system in the maturation of red blood cells in the bone marrow. Plants do not need cobalamin and carry out the reactions with enzymes that are not dependent on it.

Selenium deficiency occurs when an organism lacks the required levels of selenium, a critical nutrient in many species. Deficiency, although relatively rare in healthy well-nourished individuals, can have significant negative results, affecting the health of the heart and the nervous system; contributing to depression, anxiety, and dementia; and interfering with reproduction and gestation.

<span class="mw-page-title-main">Iodine in biology</span> Use of Iodine by organisms

Iodine is an essential trace element in biological systems. It has the distinction of being the heaviest element commonly needed by living organisms as well as the second-heaviest known to be used by any form of life. It is a component of biochemical pathways in organisms from all biological kingdoms, suggesting its fundamental significance throughout the evolutionary history of life.

<span class="mw-page-title-main">Vitamin D</span> Group of fat-soluble secosteroids

Vitamin D is a group of fat-soluble secosteroids responsible for increasing intestinal absorption of calcium, magnesium, and phosphate, and for many other biological effects. In humans, the most important compounds in this group are vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol).

References

  1. ↑ S. J. Lippard, J. M. Berg "Principles of Bioinorganic Chemistry" University Science Books: Mill Valley, CA; 1994. ISBN   0-935702-73-3.
  2. ↑ Kurokawa S, Berry MJ (2013). "Selenium. Role of the Essential Metalloid in Health". In Astrid Sigel, Helmut Sigel and Roland K. O. Sigel (ed.). Interrelations between Essential Metal Ions and Human Diseases. Metal Ions in Life Sciences. Vol. 13. Springer. pp. 499–534 Selenium. Role of the Essential Metalloid in Health. doi:10.1007/978-94-007-7500-8_16. ISBN   978-94-007-7499-5. PMC   4339817 . PMID   24470102.
  3. ↑ Bhabak Krishna P., Mugesh Govindasamy, Mugesh (2010). "Functional Mimics of Glutathione Peroxidase: Bioinspired Synthetic Antioxidants". Acc. Chem. Res. 43 (11): 1408–1419. doi:10.1021/ar100059g. PMID   20690615.
  4. ↑ Stadtman TC (1996). "Selenocysteine". Annual Review of Biochemistry. 65: 83–100. doi:10.1146/annurev.bi.65.070196.000503. PMID   8811175.
  5. ↑ "Selenium". Linus Pauling Institute at Oregon State University. 2014-04-23. Retrieved 2009-01-05.
  6. ↑ Mazokopakis EE, Papadakis JA, Papadomanolaki MG, Batistakis AG, Giannakopoulos TG, Protopapadakis EE, et al. (2007). "Effects of 12 months treatment with L-selenomethionine on serum anti-TPO Levels in Patients with Hashimoto's thyroiditis". Thyroid. 17 (7): 609–12. doi:10.1089/thy.2007.0040. PMID   17696828.
  7. ↑ H Frederik Nijhout, et al, In silico experimentation with a model of hepatic mitochondrial folate metabolism, Theoretical Biology and Medical Modeling, 2006, 3:40, link http://www.tbiomed.com/content/3/1/40/abstract).
  8. ↑ Reda T., Plugge C. M., Abram N. J., Hirst J., Plugge, Abram, Hirst (2008). "Reversible interconversion of carbon dioxide and formate by an electroactive enzyme". PNAS. 105 (31): 10654–10658. Bibcode:2008PNAS..10510654R. doi: 10.1073/pnas.0801290105 . PMC   2491486 . PMID   18667702.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ↑ Brandt W, Wessjohann LA (2005-02-04). "The Functional Role of Selenocysteine (Sec) in the Catalysis Mechanism of Large Thioredoxin Reductases: Proposition of a Swapping Catalytic Triad Including a Sec-His-Glu State". ChemBioChem. 6 (2): 386–394. doi:10.1002/cbic.200400276. ISSN   1439-7633. PMID   15651042. S2CID   25575160.
  10. ↑ Zane Davis, T. (2008). "Selenium in Plants" (PDF). p. 8. Retrieved 2008-12-05.
  11. ↑ "Selenium(IV)_sulfide". Pharmacy Codes. Retrieved 2009-01-06.
  12. ↑ "Selenium sulfide". DermNet NZ. Retrieved 2009-01-06.
  13. ↑ Allingstrup M, Afshari A (2015-07-27). "Selenium supplementation for critically ill adults". The Cochrane Database of Systematic Reviews. 2018 (7): CD003703. doi:10.1002/14651858.CD003703.pub3. ISSN   1469-493X. PMC   6517228 . PMID   26214143.
  14. ↑ R. Baselt, Disposition of Toxic Drugs and Chemicals in Man, 8th edition, Biomedical Publications, Foster City, CA, 2008, pp. 1416–1420.
  15. ↑ "Dietary Supplement Fact Sheet: Selenium". National Institutes of Health; Office of Dietary Supplements. Retrieved 2009-01-05.
  16. ↑ a report of the Panel on Dietary Antioxidants and Related Compounds, Subcommittees on Upper Reference Leves of Nutrients and of Interpretation and Use of Dietary Reference Intakes, and the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes, Food and Nutrition Board, Institute of Medicine. (August 15, 2000). Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Institute of Medicine. pp. 314–315. ISBN   978-0-309-06949-6.{{cite book}}: CS1 maint: multiple names: authors list (link)
  17. ↑ Yang G, Zhou, R. (1994). "Further Observations on the Human Maximum Safe Dietary Selenium Intake in a Seleniferous Area of China". Journal of Trace Elements and Electrolytes in Health and Disease. 8 (3–4): 159–165. PMID   7599506.
  18. ↑ Yang GQ, Xia, Yi-Ming (1995). "Studies on Human Dietary Requirements and Safe Range of Dietary Intakes of Selenium in China and Their Application in the Prevention of Related Endemic Diseases". Biomedical and Environmental Sciences. 8 (3): 187–201. PMID   8561918.
  19. ↑ "Public Health Statement: Health Effects" (PDF). Agency for Toxic Substances and Disease Registry. Retrieved 2009-01-05.
  20. ↑ Wilber CG (1980). "Toxicology of selenium". Clinical Toxicology. 17 (2): 171–230. doi:10.3109/15563658008985076. PMID   6998645.
  21. ↑ Olson, O.E. (1986). "Selenium Toxicity in Animals with Emphasis on Man". International Journal of Toxicology. 5: 45. doi: 10.3109/10915818609140736 . S2CID   74619246.
  22. ↑ Ohlendorf HM (2003). "Ecotoxicology of selenium". Handbook of ecotoxicology. Boca Raton: Lewis Publishers. pp. 466–491. ISBN   978-1-56670-546-2.
  23. ↑ Poston HA, Combs, G. F., Leibovitz, L. (1976). "Vitamin E and selenium interrelations in the diet of Atlantic salmon (Salmo salar): gross, histological and biochemical signs". Journal of Nutrition. 106 (7): 892–904. doi:10.1093/jn/106.7.892. PMID   932827.
  24. ↑ Hamilton SJ, K. J. Buhl, N. L. Faerber, R. H. Wiedmeyer, and F. A. Bullard (1990). "Toxicity of organic selenium in the diet to chinook salmon". Environ. Toxicol. Chem. 9 (3): 347–358. doi:10.1002/etc.5620090310.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  25. ↑ Ravaglia, Forti P, Maioli F, Bastagli L, Facchini A, Mariani E, et al. (1 February 2000). "Effect of micronutrient status on natural killer cell immune function in healthy free-living subjects aged >=90 y1". American Journal of Clinical Nutrition. 71 (2): 590–598. doi: 10.1093/ajcn/71.2.590 . PMID   10648276.
  26. ↑ MedSafe Editorial Team. "Selenium". Prescriber Update Articles. New Zealand Medicines and Medical Devices Safety Authority. Retrieved 2009-07-13.
  27. ↑ Ralston N, Raymond, L.J. (2010). "Dietary selenium's protective effects against methylmercury toxicity". Toxicology. 278 (1): 112–123. doi:10.1016/j.tox.2010.06.004. PMID   20561558.
  28. ↑ Mann J, Truswell AS (2002). Essentials of Human Nutrition (2nd ed.). Oxford University Press. ISBN   978-0-19-262756-8.
  29. ↑ Moreno-Reyes R, Mathieu J, Vanderpas M, Begaux F, Suetens C, Rivera MT, et al. (2003). "Selenium and iodine supplementation of rural Tibetan children affected by Kashin-Beck osteoarthropathy". American Journal of Clinical Nutrition. 78 (1): 137–144. doi: 10.1093/ajcn/78.1.137 . PMID   12816783.
  30. ↑ Institute of Medicine (2000). "Selenium". Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington, DC: The National Academies Press. pp. 284–324. doi:10.17226/9810. ISBN   978-0-309-06935-9. PMID   25077263.
  31. ↑ "Overview on Dietary Reference Values for the EU population as derived by the EFSA Panel on Dietetic Products, Nutrition and Allergies" (PDF). 2017.
  32. ↑ Tolerable Upper Intake Levels For Vitamins And Minerals (PDF), European Food Safety Authority, 2006
  33. ↑ What We Eat In America, NHANES 2001–2002 Archived 2015-01-06 at the Wayback Machine . Table A15: Selenium.
  34. ↑ "Federal Register May 27, 2016 Food Labeling: Revision of the Nutrition and Supplement Facts Labels. FR page 33982" (PDF).
  35. ↑ "Daily Value Reference of the Dietary Supplement Label Database (DSLD)". Dietary Supplement Label Database (DSLD). Archived from the original on 7 April 2020. Retrieved 16 May 2020.
  36. ↑ Barclay MN, Allan MacPherson, James Dixon (1995). "Selenium content of a range of UK food". Journal of Food Composition and Analysis. 8 (4): 307–318. doi:10.1006/jfca.1995.1025.
  37. ↑ A list of selenium-rich foods can be found on The Office of Dietary Supplements Selenium Fact Sheet.PD-icon.svg This article incorporates public domain material from this U.S government document.
  38. ↑ The most popular web reference for this is .
  39. 1 2 3 4 Razaghi A, Poorebrahim M, Sarhan D, Björnstedt M (September 2021). "Selenium stimulates the antitumour immunity: Insights to future research". European Journal of Cancer. 155: 256–267. doi: 10.1016/j.ejca.2021.07.013 . ISSN   0959-8049. PMID   34392068.
  40. ↑ Vinceti M, Filippini T, Del Giovane C, Dennert G, Zwahlen M, Brinkman M, et al. (January 29, 2018). "Selenium for preventing cancer". The Cochrane Database of Systematic Reviews. 1 (2): CD005195. doi:10.1002/14651858.CD005195.pub4. ISSN   1469-493X. PMC   6491296 . PMID   29376219.
  41. ↑ Stone CA, Kawai K, Kupka R, Fawzi WW (November 2010). "Role of selenium in HIV infection". Nutr. Rev. 68 (11): 671–81. doi:10.1111/j.1753-4887.2010.00337.x. PMC   3066516 . PMID   20961297.
  42. ↑ Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C (2012). Bjelakovic G (ed.). "Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases". Cochrane Database of Systematic Reviews (Submitted manuscript). 2012 (3): CD007176. doi:10.1002/14651858.CD007176.pub2. hdl: 10138/136201 . PMC   8407395 . PMID   22419320.
  43. ↑ Grobler L, Nagpal S, Sudarsanam TD, Sinclair D (2016). "Nutritional supplements for people being treated for active tuberculosis". Cochrane Database Syst Rev. 2016 (6): CD006086. doi:10.1002/14651858.CD006086.pub4. PMC   4981643 . PMID   27355911.
  44. ↑ Mao S, Zhang A, Huang S (2014). "Selenium supplementation and the risk of type 2 diabetes mellitus: a meta-analysis of randomized controlled trials". Endocrine. 47 (3): 758–63. doi:10.1007/s12020-014-0298-7. PMID   24858736. S2CID   22669723.
  45. ↑ Ahsan U, Kamran Z, Raza I, et al. (April 2014). "Role of selenium in male reproduction - a review". Anim. Reprod. Sci. (Review). 146 (1–2): 55–62. doi: 10.1016/j.anireprosci.2014.01.009 . PMID   24613013.
  46. ↑ Moghaddam A, Heller RA, Sun Q, Seelig J, Cherkezov A, Seibert L, et al. (July 2020). "Selenium Deficiency Is Associated with Mortality Risk from COVID-19". Nutrients. 12 (7): 2098. doi: 10.3390/nu12072098 . PMC   7400921 . PMID   32708526.
  47. ↑ Alkattan A, Alabdulkareem K, Kamel A, Abdelseed H, Almutairi Y, Alsalameen E (2021). "Correlation between Micronutrient plasma concentration and disease severity in COVID-19 patients". Alexandria Journal of Medicine. 57: 21–27. doi: 10.1080/20905068.2020.1870788 .
  48. ↑ Berry MJ, Ralston NV (2008-12-01). "Mercury Toxicity and the Mitigating Role of Selenium". EcoHealth. 5 (4): 456–459. doi:10.1007/s10393-008-0204-y. ISSN   1612-9210. PMID   19198945. S2CID   29418315.
  49. ↑ Spiller HA (2018-05-04). "Rethinking mercury: the role of selenium in the pathophysiology of mercury toxicity". Clinical Toxicology. 56 (5): 313–326. doi:10.1080/15563650.2017.1400555. ISSN   1556-3650. PMID   29124976. S2CID   4295652.
  50. 1 2 Gladyshev VN, Hatfield DL (1999). "Selenocysteine-containing proteins in mammals". Journal of Biomedical Science (Submitted manuscript). 6 (3): 151–60. doi:10.1007/BF02255899. PMID   10343164.
  51. ↑ Lobanov AV, Fomenko DE, Zhang Y, Sengupta A, Hatfield DL, Gladyshev VN (2007). "Evolutionary dynamics of eukaryotic selenoproteomes: large selenoproteomes may associate with aquatic life and small with terrestrial life". Genome Biology. 8 (9): R198. doi: 10.1186/gb-2007-8-9-r198 . PMC   2375036 . PMID   17880704.
  52. ↑ Penglase S, Hamre K, Ellingsen S (2015). "The selenium content of SEPP1 versus selenium requirements in vertebrates". PeerJ. 3: e1244. doi: 10.7717/peerj.1244 . PMC   4699779 . PMID   26734501.
  53. ↑ Castellano S, Novoselov SV, Kryukov GV, et al. (2004). "Reconsidering the evolution of eukaryotic selenoproteins: a novel nonmammalian family with scattered phylogenetic distribution". EMBO Reports. 5 (1): 71–7. doi:10.1038/sj.embor.7400036. PMC   1298953 . PMID   14710190.
  54. ↑ Kryukov GV, Gladyshev VN (2004). "The prokaryotic selenoproteome". EMBO Reports. 5 (5): 538–43. doi:10.1038/sj.embor.7400126. PMC   1299047 . PMID   15105824.
  55. ↑ Wilting R, Schorling S, Persson BC, Böck A (1997). "Selenoprotein synthesis in archaea: identification of an mRNA element of Methanococcus jannaschii probably directing selenocysteine insertion". Journal of Molecular Biology. 266 (4): 637–41. doi:10.1006/jmbi.1996.0812. PMID   9102456.
  56. ↑ Zhang Y, Fomenko DE, Gladyshev VN (2005). "The microbial selenoproteome of the Sargasso Sea". Genome Biology. 6 (4): R37. doi: 10.1186/gb-2005-6-4-r37 . PMC   1088965 . PMID   15833124.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.