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Selenium Concentration and Glutathione Peroxidase Activity in Normal and Neoplastic Development of the Mouse Mammary Gland¹

Program in Nutrition and Dietetics, University of Texas Health Science Center [H. W. L.], and Department of Cell Biology, Baylor College of Medicine [D. M.], Houston, Texas 77030

This study was divided into three experiments. (a) The levels of selenium and glutathione peroxidase (GSH-PX) activity were determined for various developmental states of the mammary gland: normal (virgin, pregnant, and lactating); preneoplastic hyperplastic outgrowth lines; and neoplastic mammary tissues. Tissues from the pregnant and lactating mice had higher selenium concentrations and GSH-PX activities than did tissues from virgin mice, but the levels were similar to levels found in preneoplastic and neoplastic mammary tissues of lines C4 and D2. This suggests that the appropriate comparisons for studies determining the effect of selenium on preneoplastic mammary tissues are glands from pregnant and lactating mice. In addition, these results suggest that the refractory state of mammary tumors to selenium-mediated growth inhibition is not due to the absence of GSH-PX or the inability to incorporate selenium. (b) For the second experiment, the effect of feeding various levels of selenium on selenium and GSH-PX levels was determined in mammary and hepatic tissues of virgin mice. GSH-PX activity increased when dietary selenium increased from less than 0.02 to 0.1 ppm selenium but was not further increased when dietary selenium was above 0.1 ppm. (c) Finally, the mammary GSH-PX activity was evaluated at different concentrations of the substrates in order to document the biochemical characteristics of the mammary gland GSH-PX.

¹ Supported by National Cancer Institute Research Grant CA-11944 and by the Science and Education Administration of the United States Department of Agriculture under Grant 5901-0401-8-0086-0 from the Competitive Research Office.

² To whom requests for reprints should be addressed.

Received 3/29/82. Accepted 1/ 4/83.

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