FAILURE OF ETHANOL METABOLITES TO ALTER GONADOTROPIN-SECRETION OR LUTEINIZING-HORMONE SYNTHESIS IN-VITRO

Citation
S. Uddin et al., FAILURE OF ETHANOL METABOLITES TO ALTER GONADOTROPIN-SECRETION OR LUTEINIZING-HORMONE SYNTHESIS IN-VITRO, Endocrine research, 21(3), 1995, pp. 653-670
Citations number
36
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
07435800
Volume
21
Issue
3
Year of publication
1995
Pages
653 - 670
Database
ISI
SICI code
0743-5800(1995)21:3<653:FOEMTA>2.0.ZU;2-T
Abstract
The impact of ethanol on the male reproductive axis are multiple and v aried, with both gonadal and control hypothalamic-pituitary pertubatio ns being reported. There appears to be a discrepancy, however, between the in vivo and in vitro effects of ethanol on hypothalamic luteinizi ng hormones releasing hormone (LHRH) and the pituitary gonadotropins l uteinizing hormone (LH) and follicle stimulating hormone(FSH). While i n vivo data suggests a decrease in LHRH release after EtOH, in vitro s tudies find no effect on secretion. Similarity, in vivo acute EtOH pro foundly diminishes LH synthesis and secretion, while in vitro impaired release with no alteration in the transcription of beta LH has been f ound. A potential exploration for these discrept results could be the in vivo metabolism of EtOH into acetaldehyde and acetate, or the subse quent formation of salsolinol, a product of acetate combining with dop amine. To test this possibility, a series of in vitro experiments were conducted exposing dispensed anterior pituitary cells from male rats to different doses of acetaldehyde, acetate or salsolinol for varying amounts of time for which gonadotropin secretion and beta LH mRNA leve ls were assessed. The results demonstrated no effect of either acetald ehyde or acetate on basal or LHRH stimulated LH release, FSH release o r steady-state beta LH mRNA levels. These data suggest that the metabo lites of EtOH, which occur in vivo but not in vitro, are not responsib le for the discrepant gonadotropin changes reported between the in viv o and in vitro setting. Other potential mechanisms to explain this phe nomenon include differences in the molarity of EtOH, hyperprolactinemi a and suprapituitary influences including hypothalamic LHRH, catechola mines, excitatory amino acids, substance P and beta endorphin.