These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Estrone and dehydroepiandrosterone sulfatase activities in guinea-pig uterus and liver: estrogenic effect of estrone sulfate.
    Author: Moutaouakkil M, Prost O, Dahan N, Adessi GL.
    Journal: J Steroid Biochem; 1984 Sep; 21(3):321-8. PubMed ID: 6593507.
    Abstract:
    Estrone and dehydroepiandrosterone (DHA) sulfatase activities were studied in the uterus and liver of female guinea-pigs (albino variety). The two activities were found in particulates, with the highest specific activity in microsomes. The effects of pH, buffers, temperature and the non-competitive inhibition of DHA sulfate on estrone sulfatase provided arguments for the existence of two distinct sulfatases. However, acrylamide gel electrophoresis of the solubilized microsome sulfatases gave a single peak for the two activities. In the uterus, the apparent Km of estrone and DHA sulfatases were 26.4 and 15.6 microM. Solubilized microsomal estrone sulfatase was inhibited by unconjugated steroids. The apparent Km of estrone sulfatase in liver was 10.7 microM. Estrone and DHA sulfatase activities were consistently lower in liver than in uterus and no DHA sulfatase activity was detected in fetal liver. In the uterus, the same sulfatase activities were found in female fetuses, castrated or mature females. Estrone sulfatase was significantly increased in the uterus of pregnant females (60-65 days gestation). Estrone sulfate was injected in vivo into mature castrated females. A significant increase in uterine weight and in uterine progesterone receptors was observed. The cytosol progesterone receptors were characterized by their Kd (1.40 nM) and by sucrose density gradient. It is concluded that the variations of estrone sulfatase activity in target tissues like the uterus may control the intracellular levels of biologically active estrogens.
    [Abstract] [Full Text] [Related] [New Search]