Attenuation of the anticarcinogenic action of selenium by vitamin E deficiency.
The present study showed that in the dimethylbenz[a]anthracene-induced mammary tumor model in rats, the anticarcinogenic efficacy of selenium was much attenuated when the intake of vitamin E was deficient. Selenium supplementation at 2.5 mg/kg in the diet reduced the total tumor yield by 45% and 25%, respectively, in rats with an adequate or low vitamin E intake. Measurements of selected hepatic phase I and phase II detoxifying enzymes indicated that they were not responsive to changes in dietary vitamin E or selenium levels. However, a low vitamin E intake significantly increased lipid peroxidation in the mammary fat pad regardless of selenium status, suggesting that selenium supplementation was less effective under this nutritional condition and might be associated with the higher degree of oxidant stress in the cellular environment.
D015127:9,10-Dimethyl-1,2-benzanthracene; D000818:Animals; D000970:Antineoplastic Agents; D005260:Female; D066298:In Vitro Techniques; D008054:Lipid Peroxides / Q000378:metabolism; D008099:Liver / Q000201:enzymology; D008325:Mammary Neoplasms, Experimental / Q000139:chemically induced / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012643:Selenium / Q000008:administration & dosage / Q000378:metabolism / Q000627:therapeutic use*; D014810:Vitamin E / Q000008:administration & dosage; D014811:Vitamin E Deficiency / Q000378:metabolism*
D000970:Antineoplastic Agents; D008054:Lipid Peroxides; D014810:Vitamin E; D015127:9,10-Dimethyl-1,2-benzanthracene; D012643:Selenium