Identification of the metabolite seleno-bis(S-glutathionyl) arsinium ion (Gailer, 2000), which allows mutual excretion of arsenic (As) and selenium (Se), raises a question: What is the physiological effect of bioavailable As if dietary Se is low, and possibly deficient? This review describes basic functions of Se-metabolites and some effects of nutritional Se-deficiencies. It suggests that physiological depletion of low dietary Se by bioavailable As may exacerbate the etiologies of several human diseases and, perhaps, those of wildlife. Descriptions of the geochemistry of either Se or As bioavailability are detailed elsewhere. Essential Se is critical as the catalytic component of glutathione peroxidase (Se-GPX) (Rotruck, 1973), a physiological antioxidant, and cellular Se-GPX is ubiquitous in prokaryotes as well as eukaryotes (Burk, 1993), including humans. Concentrations of different selenoproteins (SP), for example cSe-GPX, depend on overall Se nutrition (Patching, 1999); Se is bioavailable as inorganic Se(IV) or Se(VI), from drinking water, or as Se-amino acids selenomethionine (Se-Met) and selenocysteine (Se-Cys 1), found in many foods of plant or animal origin (Combs, 1986). Se metabolizes to essential Se-Cys from both Se(IV) and Se-Met, and less so from Se(VI). Se-Cys is the predominant active component of the various SPs (Figure 1), and it is critical (Allen, 1999) to nutrition 2. Nutritional Se-deficiencies can become manifest in any phase throughout the life cycle (Surai, 2000).
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