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Effects of Dietary Selenium on DMBA-Induced Carcinogenesis in Rats Fed a Diet High in Mixed Fats^1,2,

Mary R. L'Abbé^*,, Peter W. F. Fischer^*,, James S. Campbell and Eduardo R. Chavez

^* Nutrition Research Division Toxicology Research Division, Food Directorate, Health Protection Branch, Health and Welfare Canada, Ottawa, Ontario K1A 0L2 Department of Animal Science, Macdonald College of McGill University, Ste. Anne de Bellevue, Quebec H9X 1C0, Canada

The effects of selenium intake on 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary carcinogenesis were examined in rats fed a diet high in mixed fats and representative of that consumed in North America. Six groups of 20 rats were fed an AIN-76 diet modified to contain 20% fat from lard:corn oil (3:1 wt/wt) and various amounts of selenium (0.1, 0.035, 0.1, 1.0, 2.0 or 4.0 mg Se/kg diet). At wk 5, animals in groups 2–6 were dosed with 4.32 mg of DMBA. Serum clinical parameters and the activities of plasma selenium-dependent and total glutathione peroxidase (GSHPx), erythrocyte GSHPx and superoxide dismutase (SOD) were determined every 4 wk for 25 wk. The extent of lipid peroxidation was determined by measuring urinary malondialdehyde during wk 13 and 24, and erythrocyte malondialdehyde at wk 25. Erythrocyte GSHPx was found to be a better indicator of selenium status than plasma activity, while SOD did not vary with dietary selenium. The group of animals fed 4.0 mg Se/kg diet had reduced numbers of tumors (P < 0.01), but this reduction was associated with evidence of chronic selenium toxicity. Variations in GSHPx activity with dietary selenium did not result in differences in tumor incidence, nor in changes in lipid peroxidation in the other groups. Thus, nontoxic levels of selenium do not appear to offer any protective effect during carcinogenesis in rats fed a casein-based diet similar in fat content to that consumed by North Americans.

KEY WORDS: • selenium • cancer • fat • glutathione peroxidase • superoxide dismutase • lipid peroxidation • rat

¹ Publication No. 275 of the Bureau of Nutritional Sciences.

² Presented in part at the 29th Annual Meeting of the Canadian Federation of Biological Societies, Guelph, Ontario, June 16–20, 1986: Can. Fed. Biol. Soc. Proc. 29: 103 (abs. PA-99).

Manuscript received 14 May 1988. Revision accepted 9 February 1989.