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Modulation of Selenium-Dependent Glutathione Peroxidase by Perfluorodecanoic Acid in Rats: Effect of Dietary Selenium¹

Li-Chuan Chen^*,2, Tim Borges^*, Howard P. Glauert^{* **,}, Simon A. B. Knight^,3, Roger A. Sunde, Helga Schramm, Franz Oesch, Ching K. Chow^{* **,} and Larry W. Robertson^*

^* Graduate Center for Toxicology ^** Department of Nutrition and Food Science, University of Kentucky, Lexington, KY 40506-0054 Department of Nutrition and Food Science, University of Arizona, Tucson, AZ 85721 Institut für Toxikologie, Universität Mainz, D-6500 Mainz, West Germany

Forty-eight male Sprague-Dawley rats fed a diet containing 0.4, 0.2 or 1.0 mg of selenium (Se)/kg of diet were injected with a single dose (35 mg/kg) of perfluorodecanoic acid (PFDA) in corn oil and killed 2 wk later. Control animals were pair-fed and treated with an equal volume of vehicle. PFDA treatment significantly increased Se-dependent glutathione peroxidase (Se-GSHPx) activity in liver cytosol of rats fed the 0.04 mg of Se/kg of diet but not in rats fed the other diets. The increase in liver cytosolic Se-GSHPx activity in rats fed 0.04 mg of Se/kg of diet paralleled increases in Se content and serum Se-GSHPx activity. Determination of Se-GSHPx by an enzyme-linked immunosorbent assay showed that PFDA caused a decrease in Se-GSHPx protein in rats fed 0.2 or 1.0 mg of Se/kg of diet but not in rats fed 0.04 mg of Se/kg of diet. Further analysis revealed that the ratio of Se-GSHPx activity to antibody-reactive protein was increased by PFDA in all three groups. The in vitro addition of PFDA directly to the assay mixture for Se-GSHPx activity did not produce any effect. Reduced glutathione was significantly increased by PFDA treatment in all three groups. These data show that PFDA affects the Se content, Se-GSHPx activity and Se-GSHPx protein in rat liver and that the effect is dependent on the dietary/hepatic Se level.

KEY WORDS: • selenium • selenium-dependent glutathione peroxidase • perfluorodecanoic acid • rats

¹ Supported by American Institute for Cancer Research grant 86B66 and National Cancer Institute grant CA-43719. Kentucky Agriculture Experiment Station journal article number 89-9-124.

² To whom all correspondence should be addressed.

³ Present address: Health Science Center, Department of Internal Medicine, Endocrinology Section, University of Arizona, Tucson, AZ 85724.

Manuscript received 19 April 1989. Revision accepted 5 October 1989.

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