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IntroductionAtomic mass 79. A widely, but unevenly distributed essential micronutrient that can also be toxic in excess.ExposureSelenium is used in photoelectric cells, glass and ceramics, cosmetics, pigments and sheep dips. Occupational hazards result from exposure to dust or fume. Diets that include selenium at a rate of 1 ug per kilogram per day appear optimal. The selenium content of foodstuffs varies markedly in proportion to the selenium content of the soils in which the animal feed or cereals and vegetables have grown. Seafood provides a stable and relatively abundant source of selenium.AbsorptionSelenium absorption after inhalation of aerosol is dependent upon particle size. If the particles are respirable, most selenium will be deposited in the deep lung where soluble oxides are absorbed rapidly. Non-respired selenium is cleared to the gut. Inorganic selenium compounds are not absorbed well from the gut. Organo-selenium compounds found in cereals (mainly selenomethionine) are well absorbed.DistributionOnce absorbed organo-selenium compounds are rapidly transferred to plasma and red blood cells. Selenate, in comparison is more slowly transferred from the gut and is excluded from the red blood cells. Circulating selenium is primarily partitioned to brain, kidney and liver, but body stores are not large relative to metabolic demand. Selenium is incorporated into a range of enzymes that function as antioxidants (eg glutathione peroxidase) and in thyroid hormone metabolism.ExcretionBody balance of selenium is maintained through regulation of excretion of trimethyl selenonium to urine. Given normal intakes, about half the absorbed selenium load will be excreted to urine. In deficiency states and during pregnancy with a normal diet, very little selenium is excreted to urine. With increasing selenium body burden, selenium is exhaled as the volatile dimethyl selenide.Pathology0ccupational exposure to selenium containing fume or dust may result in eye redness, sneezing, coughing, respiratory difficulty and abdominal distress. Selenium exposure has been associated with lethal liver damage. Selenium hydride gas and selenium oxychloride liquid are both potentially lethal. Absorption of toxic doses of selenium compounds is associated with a garlic odour on the breath. Selenosis derived from exposure to selenium compounds in food and water has been associated with dental caries, dry hair, misshapen nails, skin lesions and polyneuritis.Selenium deficiency is caused by decreased dietary intake. The deficiency results in muscle abnormalities manifesting as cardiomyopathy (potentially fatal), muscle pain (commonly in the thighs) and reduced plasma glutathione peroxidase activity. Both these symptoms have been associated with long term parenteral nutrition without supplementation. MonitoringPlasma selenium levels respond rapidly to either stress (decreasing) or selenium uptake (increasing). Red cell selenium content changes more slowly in response to variations in selenium uptake and is not affected by stress. Whole blood selenium gives a good, inclusive measure of medium-term selenium status. Urinary selenium content varies markedly in normals and is subject to feeding and clearance effects that confound its use in either exposure or deficiency. Glutathione peroxidase activity in plasma may be used as a marker of selenium deficiency if selenium determinations are not available. Determinations in hair and nails are confounded by environmental contamination and so are not recommended.TreatmentSelenium deficiency is treated by diet supplementation with selenomethionine or sodium selenite.AnalysisSelenium determination may be made with graphite furnace or hydride generation atomic absorption spectrometry. PaLMS Trace Element Service employs inductively coupled plasma-mass spectrometry for improved turn around time and quality of results. |