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Although it is toxic in large doses, selenium is an essential micronutrient for animals. In plants, it occurs as a bystander mineral, sometimes in toxic proportions in forage (some plants may accumulate selenium as a defense against being eaten by animals, but other plants such as locoweed require selenium, and their growth indicates the presence of selenium in soil).[3] See more on plant nutrition below. Selenium is a component of the unusual amino acids selenocysteine and selenomethionine. In humans, selenium is a trace element nutrient that functions as cofactor for reduction of antioxidant enzymes, such as glutathione peroxidases[66] and certain forms of thioredoxin reductase found in animals and some plants (this enzyme occurs in all living organisms, but not all forms of it in plants require selenium). The glutathione peroxidase family of enzymes (GSH-Px) catalyze certain reactions that remove reactive oxygen species such as hydrogen peroxide and organic hydroperoxides: 2 GSH + H2O2----GSH-Px → GSSG + 2 H2O Selenium also plays a role in the functioning of the thyroid gland and in every cell that uses thyroid hormone, by participating as a cofactor for the three of the four known types of thyroid hormone deiodinases, which activate and then deactivate various thyroid hormones and their metabolites: the iodothyronine deiodinases are the subfamily of deiodinase enzymes that use selenium as the otherwise rare amino acid selenocysteine. (Only the deiodinase iodotyrosine deiodinase, which works on the last break-down products of thyroid hormone, does not use selenium).[67] Selenium may inhibit Hashimoto's disease, in which the body's own thyroid cells are attacked as alien. A reduction of 21% on TPO antibodies was reported with the dietary intake of 0.2 mg of selenium.[68] Increased dietary selenium intakes reduce the effects of mercury toxicity[69] and it is now recognized that the molecular mechanism of mercury toxicity involves irreversible inhibition of selenoenzymes that are required to prevent and reverse oxidative damage in brain and endocrine tissues.[70][71] Evolution in biology Main article: Evolution of dietary antioxidants From about three billion years ago, prokaryotic selenoprotein families drive the evolution of selenocysteine, an amino acid. Selenium is incorporated into several prokaryotic selenoprotein families in bacteria, archaea and eukaryotes as selenocysteine,[72] 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. One family of selenium-containing molecules (the glutathione peroxidases) destroy peroxide and repair damaged peroxidized cell membranes, using glutathione. Another 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.[73] 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.[72] 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, with the exception of vertebrates, aquatic life supports selenium utilization, whereas terrestrial habitats lead to reduced use of this trace element.[74] 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. The deiodinase isoenzymes constitute another family of eukaryotic selenoproteins with identified enzyme function. Deiodinases are able to extract electrons from iodides, and iodides from iodothyronines. They are, thus, involved in thyroid-hormone regulation, participating in the protection of thyrocytes from damage by H2O2 produced for thyroid-hormone biosynthesis.[75] About 200 Mya, new selenoproteins were developed as mammalian GSH-Px enzymes.[76][77] [78][79] Nutritional sources of selenium Dietary selenium comes from nuts, cereals, meat, mushrooms, fish, and eggs. Brazil nuts are the richest ordinary dietary source (though this is soil-dependent, since the Brazil nut does not require high levels of the element for its own needs). In descending order of concentration, high levels are also found in kidney, tuna, crab, and lobster.[80][81] The human body's content of selenium is believed to be in the 13–20 milligram range.[82] Indicator plant species 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.)[83] Medical use The substance loosely called selenium sulfide (approximate formula SeS2) is the active ingredient in some anti-dandruff shampoos.[84] 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.[85] 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.[86] 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.[87] 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.[88] 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.[89] 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.[90] 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.[91] 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.[92] Hydrogen selenide is an extremely toxic, corrosive gas.[93] 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. On 19 April 2009, 21 polo ponies died shortly before a match in the United States Polo Open. Three days later, a pharmacy released a statement explaining that the horses had received an incorrect dose of one of the ingredients used in a vitamin/mineral supplement compound that had been incorrectly compounded by a compounding pharmacy. Analysis of blood levels of inorganic compounds in the supplement indicated the selenium concentrations were ten to fifteen times higher than normal in the horses' blood samples, and 15 to 20 times higher than normal in their liver samples. It was later confirmed that selenium was the ingredient in question.[94] 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.[95] Relationship between survival of juvenile salmon and concentration of selenium in their tissues after 90 days (Chinook salmon[96]) or 45 days (Atlantic salmon[97]) exposure to dietary selenium. The 10% lethality level (LC10=1.84 µg/g) was derived by applying the biphasic model of Brain and Cousens[98] 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;[97] much above that level they die from toxic excess.[96] Deficiency Main article: Selenium deficiency Selenium deficiency is rare in healthy, well-nourished individuals. It can occur in patients with severely compromised intestinal function, those undergoing total parenteral nutrition, and[99] 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.[100] Selenium deficiency as defined by low (<60% of normal) selenoenzyme activity levels in brain and endocrine tissues occurs only when a low selenium status is linked with an additional stress, such as high exposures to mercury[101] or as a result of increased oxidant stress due to vitamin E deficiency.[102] There are interactions between selenium and other nutrients, such as iodine and vitamin E. The effect of selenium deficiency on health remains uncertain, particularly in relation to Kashin-Beck disease.[103] Also, there are interactions between selenium and other minerals, such as zinc and copper. It seems that a high dose of Se supplements to pregnant animals might disturb the Zn:Cu ratio which, in turn, leads to Zn reduction. It can be concluded that the Zn status should be monitored when high doses of Se are supplemented to pregnant animals. Further studies need to be done with higher levels of Se supplement to confirm these interactions.[104] In some regions (e.g. various regions within North America) where low available selenium levels in soil lead to low concentrations in dry matter of plants, Se deficiency in some animal species may occur unless dietary (or injected) selenium supplementation is done.[105] Ruminants are particularly susceptible. In general, absorption of dietary selenium is lower in ruminants than in non-ruminants, and is lower from forages than from grain.[106] Ruminants grazing certain forages, e.g. some white clover varieties containing cyanogenic glycosides, may have higher selenium requirements,[106] presumably because of cyanide from the aglycone released by glucosidase activity in the rumen[107] and inactivation of glutathione peroxidases due to absorbed cyanide's effect on the glutathione moiety.[108] Neonate ruminants at risk of WMD (white muscle disease) may be administered both selenium and vitamin E by injection; some of the WMD myopathies respond only to selenium, some only to vitamin E, and some to either.[109] Controversial health effects Main article: Selenium in biology A number of correlative epidemiological studies have implicated selenium deficiency (as measured by blood levels) in a number of serious or chronic diseases, such as cancer,[110] diabetes,[110] HIV/AIDS,[111] and tuberculosis. In addition, selenium supplementation has been found to be a chemopreventive for some types of cancer in some types of rodents. However, in randomized, blinded, controlled prospective trials in humans, selenium supplementation has not succeeded in reducing the incidence of any disease, nor has a meta-analysis of such selenium supplementation studies detected a decrease in overall mortality.[112] |
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