Mechanisms involved in selenium toxicity and modulation of NK cell function by selenium compounds
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Abstract
The trace element selenium (Se) was first found to be toxic in 1934 in livestock that consumed native vegetation grown in seleniferous soils of the western United States (Franke, 1934). In 1957, Schwarz and Foltz confirmed that Se was an essential nutrient for laboratory rats and over the next decade it was identified as an essential nutrient for other mammalian species (Oldfield, 1981). Since this time, Se has been confirmed as an intregal component of several enzymes and other biologically important proteins(Wendel, 1992) as well as essential for optimal immune function (Turner and Finch, 1991). Se has also been noted as possessing cancer chemopreventive activity (Schrauzer, 1992; Patterson and Levander, 1997). The cytotoxic activity of Se has been demonstrated in vitro in several tumor cell models including mouse leukemic L1210 cells (Lu et al., 1994), HT29 human colonic carcinoma cells (Stewart et al., 1997) aind human mammary tumor cells (Yan et al., 1991). Additionally, Se supplementation has been shown to reduce tumor incidence in animal models (El-Bayoumy, 1991) and in human clinical trials (Clark et al, 1996).
It has been suggested that the mechanisms involved in Se toxicity and the cancer chemopreventive activity of Se are related (Spallholz, 1994). However, the mechanisms involved have yet to be elucidated. There are a substantial amount of data that suggest that Se toxicity and the cancer chemopreventive activity of Se are both the result of the interactions between Se with thiols (Painter, 1941; Ganther, 1968). The cancer chemopreventive activity of Se has also been linked to the ability of Se supplementation to modulate immunocompetence, in particular the enhancement of natural killer (NK) cell function (Schrauzer, 1992).