Induction of Endometrial Peroxidase Synthesis and Secretion by Estrogen and Estrogen Antagonist

نویسندگان

  • Andrew Churg
  • Winston A. Anderson
چکیده

Synthesis of peroxidase was induced in the uterine epithelium of immature rats by multiple doses over a 24-96-h period of either 17 beta-estradiol, the estrogen-antagonist Parke-Davis CI-628, or a combination of estradiol plus antagonist. Endogenous peroxidase activity first appeared in the cisternae of the rough endoplasmic reticulum of surface epithelial and glandular cells within 24-48 after the initial injection. Uterine peroxidase activity was also visible in the cisternae of the Golgi apparatus, in Golgi-derived secretory granules, and within the uterine and glandular lumen. Some cells of the epithelium produced little or no peroxidase, even after 96 h. Whereas the antagonist appeared to induce synthesis and secretion of peroxidase, neither the antagonist alone nor the combined treatment (estradiol plus antagonist) reproduced the estradiol-mediated growth in organ size and increased lumen diameter.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Modulation of uterine morphology and growth by estradiol-17beta and an estrogen antagonist

The estrogen antagonist C1628 maintains sustained hypertrophy of the uterine epithelium and the synthesis of many proteins including peroxidase. C1628 is a progestogen, inducing secretion of the protein by surface epithelial and glandular cells. C1628 is a connective tissue mitogen, inducing DNA synthesis in fibroblasts and the endothelium. C1628 and estrogen share these properties mentioned ab...

متن کامل

The Effects of Estrogen Receptors' Antagonist on Brain Edema, Intracranial Pressure and Neurological Outcomes after Traumatic Brain Injury in Rat

Background: In previous studies, the neuroprotective effect of 17&beta-estradiol in diffuse traumatic brain injury has been shown. This study used ICI 182,780, a non-selective estrogen receptor antagonist, to test the hypothesis that the neuroprotective effect of 17&beta-estradiol in traumatic brain injury is mediated by the estrogen receptors. Methods: The ovariectomized rats were divided into...

متن کامل

بررسی ایمونوهیستوشیمی بروز گیرنده‌های استروژن و پروژسترون در انواع هیپرپلازی و کارسینوم آندومتریویید آندومتر

Background: Endometrial carcinoma (EC) is the most common gynecologic malignancy however, mechanisms underlying its pathogenesis remain obscure. Endometrial carcinoma has been classified into two major categories: type I (related to estrogen or endometrioid adenocarcinoma) and type II (unrelated to estrogen). Estrogen is the main trigger for the abnormal proliferation in the endometrial epithel...

متن کامل

Role of melatonin receptors in the effect of estrogen on brain edema, intracranial pressure and expression of aquaporin 4 after traumatic brain injury

Objective(s): Traumatic brain injury (TBI) is one of the most common causes of death and disability in modern societies. The role of steroids and melatonin is recognized as a neuroprotective factor in traumatic injuries. This study examined the role of melatonin receptors in the neuroprotective effects of estrogen. Materials and Methods: Seventy female ovariectomized Wistar rats were divided in...

متن کامل

Pnm-12: Endometriosis and Diet Control

Background: Endometriosis, defined as the presence of endometrial tissue outside the uterus, is one of the common gynecological disorders which affect about 10% of the women in the general population. This benign condition is associated with dysmenorrhea, dyspareunia, chronic pelvic pain and infertility but may also be completely asymptomatic in some cases. Endometriosis is the common reason of...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • The Journal of Cell Biology

دوره 62  شماره 

صفحات  -

تاریخ انتشار 1974