Comparison of ovariectomy and retinyl acetate on the growth of established 7,12-dimethylbenz[a]anthracene-induced mammary tumors in the rat.
Prolonged exposure to retinyl acetate (RA) in the diet inhibits the development of 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary cancers in rats. The effectiveness of RA was examined when given 6 months after the administration of DMBA. Non-inbred female Sprague-Dawley rats with DMBA-induced mammary tumors were divided into 3 groups and treated for 4 weeks as follows: Group 1 served as controls, group 2 was ovariectomized, and group 3 received 328 mg RA/kg diet. Ovariectomy (OVX) markedly reduced both the number and size of the tumors. RA administration failed to induce any significant regression in tumor number but significantly retarded tumor growth when compared to tumor growth in group 1 controls. The levels of estradiol, progestin, and prolactin ( PRL) receptors were significantly reduced after OVX, whereas only the levels of PRL receptors declined significantly after RA administration. Circulating progesterone concentrations were not affected in the RA-treated group but the plasma PRL level was significantly increased. The present studies show that if treatment with RA is delayed until 6 months after carcinogen administration, the protective effect of RA can still be observed although its effectiveness is less dramatic than when it is administered earlier.[1]References
- Comparison of ovariectomy and retinyl acetate on the growth of established 7,12-dimethylbenz[a]anthracene-induced mammary tumors in the rat. Gandilhon, P., Melancon, R., Djiane, J., Kelly, P.A. J. Natl. Cancer Inst. (1982) [Pubmed]
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