THE EFFECT OF ACUTE INVIVO ETHANOL EXPOSURE ON FOLLICLE-STIMULATING-HORMONE TRANSCRIPTION AND TRANSLATION

The impact of ethanol (EtOH) on male rodent reproduction has been well characterized for luteinizing hormone (LH) with suppression of LH release from the pituitary being reported. We have previously reported that acute ethanol (EtOH) exposure in vivo results in rapid and marked suppression of beta-L...

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Veröffentlicht in:Alcoholism, clinical and experimental research clinical and experimental research, 1992-08, Vol.16 (4), p.776-780
Hauptverfasser: EMANUELE, MA, TENTLER, JJ, HALLORAN, MM, EMANUELE, NV, WALLOCK, L, KELLEY, MR
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Sprache:eng
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Zusammenfassung:The impact of ethanol (EtOH) on male rodent reproduction has been well characterized for luteinizing hormone (LH) with suppression of LH release from the pituitary being reported. We have previously reported that acute ethanol (EtOH) exposure in vivo results in rapid and marked suppression of beta-LH gene expression and protein release from the pituitary. This suppression of beta-LH gene expression was unaccompanied by a change in the common alpha-subunit mRNA. To further explore the impact of ethanol on male rodent reproduction, we have expanded our studies to follicle stimulating hormone (FSH) and hypothalamic luteinizing hormone releasing hormone (LHRH) as well as of pituitary protein kinase C (PKC). Previously castrated male rats were acutely exposed to EtOH and a dramatic reduction in both serum FSH and LH levels was noted at 1.5 and 3 hr after treatment. These levels returned to saline injected control values at 6 and 24 hr. Despite the fall in serum FSH, there was no change in intrapituitary FSH content at any time point; this lack of pituitary FSH depletion in the face of a fall in serum levels is suggestive of impaired FSH release. In contrast to the fall in beta-LH steady-state mRNA levels seen previously and confirmed in the present studies, there was no change in beta-FSH steady-state mRNA at any time point suggesting that EtOH has dichotomous effects on the expression of these two gonadotropins. Pituitary PKC levels were also assessed and found to be unaffected by EtOH at any time point. This enzyme is important in transmembrane signaling for the gonadotropins, and while ETOH is known to affect PKC in other cells, it appears that the effect of EtOH on the gonadotrops is not mediated at this level. Finally, hypothalamic luteinizing hormone releasing hormone (LHRH) content was assessed by radioimmunoassay, and no change was found at any time point in this hypothalamic peptide. We conclude that the effect of EtOH on pituitary gonadotropin gene expression is not uniform, with beta-LH suppression occurring selectively while beta-FSH is unaltered. The release of both gonadotropins appears to be impaired by EtOH, while pituitary PKC and hypothalamic LHRH content are unchanged.
ISSN:0145-6008
DOI:10.1111/j.1530-0277.1992.tb00677.x