Abstract:
Selenium (Se) is an essential micronutrient in animals, plants, and microorganisms; however, Se is harmful in excess, and there is a narrow range between deficiencies and toxicity in humans. Se is incorporated into various proteins either nonspecifically by replacing amino acids with their Se counterpart or specifically through selenocysteine incorporation into synthesized polypeptide chains forming selenoproteins. Well-known roles of selenoproteins include antioxidant function, immune regulation, hormone regulation, and reproduction. Five selenoproteins—glutathione peroxidase (GPX)4, thioredoxin reductase (Txnrd)1, Txnrd2, iodothyronine deiodinase (Dio)3, and selenoprotein P (Sepp1)—are considered “essential” based on the triage theory, where preference is given for their production for short-term survival and/or reproduction. GPX1, GPX2, GPX3, Dio1, Dio2, methionine sulfoxide reductase B1, and selenoprotein N (SelN) are considered as “non-essential” selenoproteins, the activities of which are preferentially lost in a modest Se deficiency. Age-related diseases such as cancer, immune dysfunction, and heart disease are considered partly due to modest Se deficiencies which decreases the expression and activities of such non-essential selenoproteins. The mechanisms of action of Se in life include epigenetic modulation, apoptosis, cell cycle arrest, and induction of reactive oxygen species. General recommendations for selenium to support human health are intake levels leading to serum concentrations of 120–150 ng/mL. Individual Se requirements, however, vary considerably with demographic, lifestyle, health, endogenous DNA stability, and genetic factors.