The effect of acute in vivo ethanol exposure on follicle stimulating hormone transcription and translation

M. A. Emanuele, J. J. Tentler, M. M. Halloran, N. V. Emanuele, L. Wallock, Mark Kelley

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish (US)
Pages (from-to)776-780
Number of pages5
JournalAlcoholism: Clinical and Experimental Research
Volume16
Issue number4
StatePublished - 1992
Externally publishedYes

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Follicle Stimulating Hormone
Transcription
Luteinizing Hormone
Ethanol
Hypothalamic Hormones
Protein Kinase C
Gonadotropins
Gene expression
Gonadotropin-Releasing Hormone
Gene Expression
Messenger RNA
Reproduction
Rodentia
Serum
Pituitary Gonadotropins
Pituitary Hormones
Radioimmunoassay
Rats
Peptides
Enzymes

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Toxicology

Cite this

The effect of acute in vivo ethanol exposure on follicle stimulating hormone transcription and translation. / Emanuele, M. A.; Tentler, J. J.; Halloran, M. M.; Emanuele, N. V.; Wallock, L.; Kelley, Mark.

In: Alcoholism: Clinical and Experimental Research, Vol. 16, No. 4, 1992, p. 776-780.

Research output: Contribution to journalArticle

Emanuele, M. A. ; Tentler, J. J. ; Halloran, M. M. ; Emanuele, N. V. ; Wallock, L. ; Kelley, Mark. / The effect of acute in vivo ethanol exposure on follicle stimulating hormone transcription and translation. In: Alcoholism: Clinical and Experimental Research. 1992 ; Vol. 16, No. 4. pp. 776-780.
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abstract = "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.",
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T1 - The effect of acute in vivo ethanol exposure on follicle stimulating hormone transcription and translation

AU - Emanuele, M. A.

AU - Tentler, J. J.

AU - Halloran, M. M.

AU - Emanuele, N. V.

AU - Wallock, L.

AU - Kelley, Mark

PY - 1992

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N2 - 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.

AB - 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.

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