ABSTRACT
Selenium (Se) is required in selenocysteine (Sec), the 21st genetically encoded amino acid and the most potent physiological nucleophile. Few environmental stressors impair selenoenzyme activities in the brain. However, as the strongest intracellular nucleophile, Sec is vulnerable to binding by electron poor soft electrophilic chalcophiles, i.e. metals, metalloids, nonmetals, and certain organic molecules. Selenoenzymes prevent and reverse oxidative damage to lipids and proteins, support immune functions, assist in regulating calcium and thyroid hormone metabolism, tubulin polymerization, protein folding, regulate Se transport in the body, and one is required for Sec synthesis. Neuroendocrine tissues are selectively supplied with Se to support Sec synthesis, so dietary deprivation is usually without overt consequences but does accentuate toxicity of soft electrophiles. Exacerbating effects of accentuated electron poor soft electrophilic chalcophiles intakes, particularly in Se-poor populations, may affect pathogenic disease progression and could increase their mutation rates, thus contributing to promulgation of novel strains in Se-poor regions of the world.
