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Dietary Selenite Modifies Glutathione Metabolism and 7,12-Dimethylbenz(a)anthracene Conjugation in Rats^1,2,3,

Department of Nutrition, The Pennsylvania State University, University Park, PA 16802

The present studies determined the impact of dietary selenite on glutathione homeostasis in liver and mammary tissue and its relationship to biliary excretion of 7,12-dimethylbenz(a)anthracene (DMBA) conjugates. In Experiment 1, liver and mammary tissue concentration of reduced glutathione (GSH) and activities of -glutamylcysteine synthetase (GCS), glutathione reductase (GR) and glutathione S-transferases (GST) were positively correlated with tissue selenium concentration in female rats fed semipurified diets supplemented with sodium selenite (0.05 to 4 mg Se/kg). The magnitude of the response was dependent upon total selenite intake and the tissue examined. Glutathione peroxidase activity did not correlate with tissue GSH concentration. Because both selenite and BHT have been reported to elevate liver GSH, Experiment 2 compared these agents (4 mg Se/kg and 6 g/kg BHT/kg, respectively) on the biliary excretion of DMBA metabolites. Five major biliary DMBA conjugates, three GSH and two ß-glucuronide, were identified. Dietary addition of selenite or BHT enhanced the excretion of these DMBA conjugates by over 100% during the 15-h collection period. These investigations suggest that dietary selenium can alter the concentration of GSH and the activities of three glutathione-dependent enzymes in mammary and liver, accounting for part of the expanded biliary excretion of DMBA conjugates. Enhanced biliary loss of DMBA conjugates likely relates to the reported depression in DMBA binding to mammary cell DNA and the inhibition of DMBA carcinogenesis caused by dietary selenite.

KEY WORDS: • selenite • glutathione • rats • mammary • bile

¹ Presented in part at the Annual Meeting of the Federation of American Societies for Experimental Biology, April 1992, Anaheim, CA [Milner, J. A., Liu, J. Z. & Zhang, B. Z. (1992) Dietary selenium increases glutathione content and glutathione S-transferase activity in rat liver and mammary tissue. FASEB J. 6: A1366 (abs.)].

² Supported in part by NIH grant CA 44567.

³ The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

⁴ Current address: Department of Internal Medicine, Affiliated Hospital of Shandong Medical University, Jinan, Shandong, 250012, the People's Republic of China.

⁵ To whom correspondence and reprint requests should be addressed.

Manuscript received 5 March 1993. Revision accepted 22 September 1993.

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