Selenium inhibition of chemical carcinogenesis.
In this article I review the work of our laboratory concerning the relationship between dietary Se intake and susceptibility to mammary carcinogenesis induced by 7,12-dimethylbenz[a]anthracene in female rats. The effect of graded levels of Se in the diet was investigated, ranging from deficiency to excessive supplementation that produced marginal toxicity in the animals. In addition, the interdependence between Se status and fat intake was also explored. Further experiments were aimed at defining the role of Se in the initiation and promotion phases of chemical carcinogenesis. In view of the biochemical function of Se as an antioxidant, the chemopreventive efficacy of Se was compared to that of vitamin E in conjunction with their ability to inhibit lipid peroxidation. Results of this study indicated that the antitumorigenic activity of Se could not be accounted for by suppression of tissue peroxidation, although an environment with a lower oxidant stress might enhance the potency of Se in protecting against cancer. The possible mechanisms of action of Se based on the observations and characteristics of several tumor models are briefly discussed.
D015127:9,10-Dimethyl-1,2-benzanthracene; D000273:Adipose Tissue / Q000201:enzymology / Q000378:metabolism; D000818:Animals; D004032:Diet; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D008054:Lipid Peroxides / Q000378:metabolism; D008099:Liver / Q000201:enzymology / Q000378:metabolism; D008325:Mammary Neoplasms, Experimental / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D011230:Precancerous Conditions / Q000139:chemically induced / Q000517:prevention & control; D051381:Rats; D012643:Selenium / Q000172:deficiency / Q000494:pharmacology*; D014810:Vitamin E / Q000494:pharmacology
D008054:Lipid Peroxides; D014810:Vitamin E; D015127:9,10-Dimethyl-1,2-benzanthracene; D005979:Glutathione Peroxidase; D012643:Selenium