Selenium and mouse mammary tumorigenesis: an investigation of possible mechanisms

The effects of selenium on 7,12-dimethylbenzanthracene-induced mammary tumorigenesis were examined in C57BL X DBA/2f F1 mice fed a semipurified diet. Mice fed 0.2 ppm selenium developed 56% mammary tumors; in contrast, mice fed 2.0 ppm selenium developed only 16% mammary tumors at 11 months of age....

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Bibliographic Details
Published in:Cancer research (Chicago, Ill.) Ill.), 1983-05, Vol.43 (5 Suppl), p.2460s
Main Authors: Medina, D, Lane, H W, Tracey, C M
Format: Article
Language:English
Subjects:
9,10-Dimethyl-1,2-benzanthracene
Animals
Benz(a)Anthracenes
Cell Division - drug effects
Cell Line
Drug Interactions
Female
Mammary Neoplasms, Experimental - chemically induced
Mammary Neoplasms, Experimental - prevention & control
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Inbred DBA
Selenium - pharmacology
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Summary:The effects of selenium on 7,12-dimethylbenzanthracene-induced mammary tumorigenesis were examined in C57BL X DBA/2f F1 mice fed a semipurified diet. Mice fed 0.2 ppm selenium developed 56% mammary tumors; in contrast, mice fed 2.0 ppm selenium developed only 16% mammary tumors at 11 months of age. Mice fed the 2.0-ppm selenium diet grew as well as did their counterparts fed the 0.2-ppm selenium diet. In a separate experiment, the level of selenium-dependent glutathione peroxidase was measured in the mammary glands of control and 7,12-dimethylbenzanthracene-treated BALB/c mice fed basal and selenium-supplemented diets. 7,12-Dimethylbenzanthracene treatment resulted in decreased glutathione peroxidase activity n mice fed both low (0.03 ppm)- and high (1.50 ppm)-selenium diets. Thus, the chemopreventive effects of selenium could not be attributed to maintaining high levels of glutathione peroxidase. In a second series of experiments, the effects of selenium were further examined on the growth of mammary cell line YN-4 in monolayer cell culture. The mitochondrial inclusions seen in cells exposed to 5 X 10(-6) M selenium could not be correlated with changes in the activity of the mitochondrial enzymes, cytochrome c oxidase and succinate dehydrogenase, thus implying that there was no demonstratable impairment of mitochondria. The examination of selenium-treated cells with flow cytofluorometry indicated that cells were blocked in S-G2 phases of the cell cycle. This latter result illustrates one feasible approach towards identifying specific mechanisms for the chemopreventive effects of selenium.
ISSN:0008-5472