help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Alhadi, T.
Right arrow Articles by Vonderhaar, B. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Alhadi, T.
Right arrow Articles by Vonderhaar, B. K.

Endocrinology, Vol 110, 254-259, Copyright © 1982 by Endocrine Society


ARTICLES

Induction of cryptic lactogenic hormone binding in livers of adult female mice treated neonatally with estradiol or nafoxidine

T Alhadi and BK Vonderhaar

Female mice were treated with 25 micrograms of either estradiol-17 beta or the antiestrogen Nafoxidine (U11100A) or sesame oil carrier within 36 h of birth. The former treatments result in persistently elevated serum PRL levels in the adult animals. Therefore, when the mice reached maturity (3-6 months of age), their livers were examined for the level of lactogenic binding. When microsomal preparations were examined for their ability to bind either lactogenic hormone, PRL, or hGH, no differences in the control or treated groups were observed. The presence of masked or cryptic binding sites were observed. The presence of masked or cryptic binding sites was examined by either solubilization of the membrane preparations or by treatment with the methyl donor S-adenosyl-L-methionine. In all cases cryptic sites were present. In control animals unmasking of cryptic binding sites produced an increment in binding of 20-60%, but in the estradiol-17 beta- and Nafoxidine-treated animals, a 120-170% increase in binding sites was observed with no significant changes in Ka. These increases observed in the latter groups are similar to the 94-175% increase seen in livers of late pregnant and lactating mice. Thus, the persistently high serum PRL levels in neonatally treated mice result in the induction of hepatic lactogenic receptors, primarily in a masked or cryptic form.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1982 by The Endocrine Society