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The Effect of Acute in Vivo Ethanol Exposure on Follicle Stimulating Hormone Transcription and Translation
Author(s) -
Emanuele M. A.,
Tentler J. J.,
Halloran M. M.,
Emanuele N. V.,
Wallock L.,
Kelley M. R.
Publication year - 1992
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1992.tb00677.x
Subject(s) - medicine , endocrinology , luteinizing hormone , follicle stimulating hormone , hormone , gonadotropic cell , in vivo , gene expression , biology , chemistry , gene , microbiology and biotechnology , biochemistry
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 β‐LH gene expression and protein release from the pituitary. This suppression of β‐LH gene expression was unaccompanied by a change in the common α‐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 β‐LH steady‐state mRNA levels seen previously and confirmed in the present studies, there was no change in β‐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 β‐LH suppression occurring selectively while β‐FSH is unaltered. The release of both gonadotropins appears to be impaired by EtOH, while pituitary PKC and hypothalamic LHRH content are unchanged.