Urinary Excretion of Selenium (Se) and Trimethyl-selenonium (TMSe) by NZ Women During Long Term Supplementation with Selenate or Selenomethionine (Semet)

The unusual situation in New Zealand adds one more variable to our understanding of how selenium is metabolized, though the problem is complicated by the scarcity of information about dietary forms, functions, metabolism and excretion. We had noted that New Zealanders, and also the Chinese in Keshan disease areas, excreted a smaller proportion of the selenium presented to their kidneys, i.e., they had lower renal plasma clearances, than North American residents (Robinson et al. 1985). Evidence of urinary metabolites is scanty, although it is almost 20 years since Byard (1969) and Palmer et al. (1969) identified trimethyl selenonium (TMSe) in rat urine; a major metabolite when the diet was relatively high in Se (>0.5 ppm Se), but minor when the urine was low in Se. Although TMSe has been identified in human urine (Burk 1976), its importance is not clear, varying from less than 1 to 50% of total Se in the urine, partly because of the difficulty in separating TMSe by the HPLC, dual column, or reineckate methods or a combination of these, and ultimately estimating it precisely.