Effect of Dietary Selenium on the Induction of Altered Hepatic Foci and Hepatic Tumors by the Peroxisome Proliferator Ciprofibrate

Howard P. Glauert, Mark M. Beaty

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

The purpose of this study was to determine if the dietary antioxidant selenium could inhibit hepatocarcinogenesis induced by peroxisome proliferators, which are hypothesized to induce tumors by increased production of hydrogen peroxide or other reactive oxygen species. Rats were fed diets containing the peroxisome proliferator ciprofibrate and one of three concentrations (0.04, 0.2, or 1.0 ppm) of selenium for 6 or 21 months. The incidence of hepatic tumors and the number and volume of γ-glutamyl transpeptidase-positive, A TPase-negative, glucose-6-phosphatase-negative, and gtucose-6-phosphatase-positivefoci at 21 months were lower in rats fed higher levels of selenium (no foci or tumors were seen at 6 mo). Indices of oxidative damage in the liver (thiobarbituric acid reactants, conjugated dienes, and lipidsoluble fluorescence products), however, were not decreased in rats fed the high-selenium diet. Therefore, selenium was protective against ciprofibrate-induced hepatocarcinogenesis, but not by reducing the degree of oxidative damage. The liver selenium and glutathione concentrations, and liver selenium-dependent glutathione peroxidase activity, increased as dietary selenium increased. Therefore, inhibition of carcinogenesis by selenium was correlated with increased levels of glutathione and glutathione peroxidase, but these did not inhibit the indices of oxidative damage. Peroxisomal s-oxidation also increased with the dietary selenium content; it therefore does not appear to be a factor in the inhibition of hepatocarcinogenesis in rats fed higher levels of selenium.

Original languageEnglish
Pages (from-to)261-271
Number of pages11
JournalNutrition and Cancer
Volume14
Issue number3-4
DOIs
StatePublished - Jan 1990

Bibliographical note

Funding Information:
The authors thank Dr. Harold Campbell, University of Wisconsin (Madison, WI) for his invaluable help in the set-up and use of the computer system for quantifying altered hepatic foci and Brian Mason, Suseela Srinivasan, Tim Borges, Li-Chuan Chen, Vickie Tatum, Manjushree Karkare, Travis Lay, and Patrick Comer for technical assistance. This paper is Kentucky Agricultural Experiment Station (journal) article no. 89-9-134. This work was supported by American Institute for Cancer Research (Washington, DC) Grant No. 86B66 and National Cancer Institute, National Institutes of Health (Bethesda, MD) Grant No. CA-43719. Address reprint requests to Dr. H. P. Glauert, Univ. of Kentucky, Dept. of Nutrition and Food Science, 212 Funkhouser Blvd., Lexington, KY 40506-0054.

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Oncology
  • Nutrition and Dietetics
  • Cancer Research

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