Inactivation of Estrogen by Rat Uterine Preparations

Publisher Website
Google Scholar
Abstract
Estradiol was inactivated by H2O2 and a 1.2M NaCl extract of a rat uterine participate preparation. The reaction was stimulated by dichlorophenol and was inhibited by low molecular weight components of the uterine supernatant fraction, by ascorbic acid, DPNH, TPNH, epinephrine, methimazole, sodium azide and to a lesser extent by reduced glutathione and sodium cyanide. Inactivation was produced by extracts prepared from ovariectomized estrogen-injected animals but not from ovariectomized animals not pretreated with estrogen. The administration of progesterone decreased the estradiol-inactivating activity of the ovariectomized estrogenprimed animals. Extracts prepared from animals in estrus had considerably greater estradiol inactivating activity than extracts prepared from animals in diestrus. Extracts from immature animals and from animals late in pregnancy did not inactivate estradiol, whereas extracts from animals early in pregnancy had decreased estrogen-inactivating activity. Estradiol 17-acetate and stilbestrol, but not estradiol 3-acetate, also were inactivated by this sytem. H2O2 could be replaced by glucose and glucose oxidase, by FMN and light, and by Mn++ and either a TPNH- or a DPNHgenerating system. Estradiol was inactivated by H2O2 and an extract of rat peritoneal lavage leukocytes rich in eosinophils. Estradiol was inactivated by H2O2 and relatively high concentrations of methemoglobin, metmyoglobin and ferricytochrome C. These results are discussed with particular regard to the role of tissue eosinophils as the source of the uterine peroxidase. (Endocrinology76: 301, 1965)