Selenium--its biological perspectives.

Abstract

Selenium is an essential trace element at lower concentrations and toxic at higher concentration. Animals can metabolize both inorganic and organic forms and convert non methylated Se to mono--or di--or tri--methylated forms, of which, mono-methylated forms are most toxic. Glutathione reductase converts selenoglutathione to H2S in liver and erythrocytes and is ultimately excreted. Se effects the toxicities of xenobiotic agents, provides antagonistic effect to Sulphur and co-administration with Zn increase Se retention in certain organs. At its toxic level (4-8 ppm) it increases Cu contents of heart, liver and kidney and has detoxifying or protecting effect against Cd and Hg. It is a prosthetic group of several seleno metalloenzymes. The concentration of the element is decreased in serum/plasma or erythrocytes of patients of AIDS, trisomy-21, Crohn's and Down's syndrome, phenylketonurea, Keshan's disease and cancer. Rather, the element has antiproliferative and cancer protecting effect. Se content of testes increases considerably during pubertal maturation and, during Se deficiency, the supply to the testes has priority over the other tissues. The element is localized in the mitochondrial capsule protein (MCP) and is involved in biosynthesis of testosterone. Neither the age of mother nor the concentration of Se during pregnancy has any effect on weight of baby or the length of pregnancy. Se levels in human milk is affected by maternal intake and its requirements by infants and young children are higher for their rapid growth. Clinical symptoms of its toxicity include severe irritations of respiratory system, metallic taste in mouth, formication of nose, signs of rhinitis, lung edema and brancho-pneumonia. The typical garlic odour of breath and sweat is due to dimethyl-selenide.