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Department of Physiology and Biophysics, University of Tennesse Medical Units, Memphis, Tennessee 38103
Intact, ovariectomized, and hypophysectomized female Sprague-Dawley rats were sacrificed at various intervals after the administration of 9,10-dimethyl-1,2-benzanthracene-(DMBA)-9-14C. The abdominal-inguinal mammary glands from the right side of the rat were used to determine the radioactivity contained within the mammary teat, fat pad, and vascular areas, while those from the left side were separated into parenchymal cell and fat cell fractions. The intracellular lipid of the parenchymal cells was extracted and quantitated. Although the pattern of carcinogen uptake and clearance by the parenchymal cell intracellular lipid was similar in all 3 groups, a greater concentration of DMBA was found in the fraction obtained from ovariectomized and hypophysectomized rats sacrificed at the later time periods. These data indicated that the intracellular lipid of the parenchymal cell is important in the uptake of carcinogen by ovariectomized and hypophysectomized rats, as well as in intact rats. Furthermore, endocrine alteration of parenchymal cell uptake of carcinogen may have resulted from changes in the amount of parenchymal cell intracellular lipid and not in changes in the amount of lipid in the mammary gland fat pad. The specific activity of the dry, fat-free parenchymal cell residue of intact rats was maintained at higher levels than the residue of either ovariectomized or hypophysectomized rats. It appeared that the DMBA was bound to some cellular component(s) of mammary parenchyma in all 3 groups of animals. However, the degree of carcinogen binding and the maintenance of bound carcinogen within the parenchymal cells of ovariectomized and hypophysectomized rats appeared to be altered. Although this investigation does not explain the modification of DMBA-induced mammary carcinogenesis resulting from ovariectomy and hypophysectomy, it does suggest that it may be the result of alterations in the metabolism and/or binding of carcinogen by the parenchymal cell.
1 This investigation was supported in part by USPHS Research Grant CA-05105 from the National Cancer Institute, The Jane Coffin Childs Memorial Fund for Medical Research Project 222, and The American Cancer Society Institutional Grant 85-C.
2 USPHS Trainee (GM-00352). Present address: Veterans Administration Hospital, Memphis, Tenn. 38104.
3 Lederle Medical Faculty Awardee.
Received 5/11/71. Accepted 7/28/71.
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