EBM Email Content Delivery
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
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 reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Karanth, S.
Right arrow Articles by McCann, S. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Karanth, S.
Right arrow Articles by McCann, S. M.
Experimental Biology and Medicine 229:926-934 (2004)
© 2004 Society for Experimental Biology and Medicine

ORIGINAL RESEARCH ARTICLE

17ß-Estradiol Stimulates Ascorbic Acid and LHRH Release from the Medial Basal Hypothalamus in Adult Male Rats

Sharada Karanth1, Wen H. Yu, Claudio M. Mastronardi and Samuel M. McCann

Pennington Biomedical Research Center (Louisiana State University), Baton Rouge, Louisiana 70808–4124

To whom requests for reprints should be addressed at 1 5435 Essen Lane #5, Baton Rouge, LA 70809. E-mail: skaranth{at}cox.net

In the present investigation, 17ß-estradiol (E2) and tamoxifen, an antiestrogen, were evaluated for their effects on the release of ascorbic acid (AA) and luteinizing hormone-releasing hormone (LHRH). Medial basal hypothalami (MBH) from adult male rats were incubated with graded concentrations of E2 (10 –9 to 10–6 M) or a combination of E2 (10–7 M) and tamoxifen (10–7 and 10–6 M ) in 0.5 ml of Krebs Ringer bicarbonate buffer for 1 hr. AA and LHRH in the incubation medium were measured by high-performance liquid chromatography and radioimmunoassay, respectively. E2 significantly elevated both AA and LHRH release and the minimal effective dose was 10–7 M. A combination of E2 (10–7 M) and tamoxifen (10–6 M) totally blocked E2-induced AA and LHRH release. The stimulatory effect of E2 was also suppressed in the presence of NG-monomethyl-L-arginine, a competitive inhibitor of nitric oxide synthase (NOS), illustrating that the release is mediated by nitric oxide (NO). To further characterize the role of NO, the tissues were incubated with E2 or a combination of E2 + (6 anilino-5, 8-quinolinedione) LY 83583 (10–6 and 10–5 M), an inhibitor of NOS. LY 83583 was effective in suppressing E2-induced AA and LHRH release, demonstrating that the effect was mediated by cyclic GMP. Incubation of the tissues with E2 or a combination of E2 + 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (O.D.Q.) (10–5 and 10–4 M), a specific inhibitor of soluble guanylyl cyclase failed to alter AA release but significantly suppressed LHRH release. The role of a prostaglandin synthesis blocker in E2-induced AA and LHRH release was tested by incubating the tissues with E2 or a combination of E2 + indomethacin (1.8 x 10 –7 or 1.8 x 10–6 M). Indomethacin produced a significant decrease in E2-induced AA and LHRH release, suggesting that the release process required prostaglandins as an intracellular mediator. In conclusion, E2 stimulated both AA and LHRH release and the effect was mediated by NO and prostaglandins.

Key Words: tamoxifen • LY 83583 (NOS inhibitor) • O.D.Q (GC inhibitor) • indomethacin






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2004 by the Society for Experimental Biology and Medicine.