Activation by human chorionic gonadotropin of ovarian carbonyl reductase in mature rats exposed in vivo to estrogens

We investigated the effects of exogenous estrogens and human chorionic gonadotropin (hCG) on the activity, content, and immunohistochemical localization of ovarian carbonyl reductase (CR) in mature cycling rats. Estrogens, estradiol, hexestrol (HEX) and diethylstilbestrol (DES) were given s.c. to ra...

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Published inBiochemical pharmacology Vol. 47; no. 9; pp. 1489 - 1496
Main Authors Inazu, Norihisa, Satoh, Tetsuo
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 29.04.1994
Elsevier Science
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Summary:We investigated the effects of exogenous estrogens and human chorionic gonadotropin (hCG) on the activity, content, and immunohistochemical localization of ovarian carbonyl reductase (CR) in mature cycling rats. Estrogens, estradiol, hexestrol (HEX) and diethylstilbestrol (DES) were given s.c. to rats daily for 3 days from the first day of diestrus, and hCG was given s.c. at 3:00 p.m. on the day of expected proestrus. The ovaries were isolated on the day of expected estrus. Ovarian CR activity was measured by using two substrates that reflect the activity of the enzyme in rats, and the enzyme content was determined by western blot analysis. Ovarian CR activity and content were decreased by estrogens as well as by inhibition of ovulation; hCG restored both the activity and the content decreased by estrogens to levels produced by nGC alone. Nevertheless, the number of ova in the oviduct when ovulation was decreased or blocked by estrogens was not restored completely by hCG treatment. Faint immunostaining in the interstitial gland cells of HEX-treated rat ovaries was observed. These results suggest that (i) although hCG activates ovarian CR in estrogen-treated rats, this increase in both enzyme activity and content may not be an obligatory event in the ovulatory process, and (ii) exogenous estrogens may predominantly influence the ovarian CR in the interstitial gland cells in mature rats by inhibiting luteinizing hormone release from the pituitary.
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ISSN:0006-2952
1873-2968
DOI:10.1016/0006-2952(94)90522-3