The effect of acute in vivo ethanol exposure on follicle stimulating hormone transcription and translation.
The effect of acute in vivo ethanol exposure on follicle stimulating hormone transcription and translation.
复制标题
体内急性乙醇暴露对卵泡刺激激素转录和翻译的影响。
DOI：
10.1111/j.1530-0277.1992.tb00677.x
复制
发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Kelley,MR
中科院分区：
文献类型：
--
作者：
Emanuele,MA;Tentler,JJ;Halloran,MM;Emanuele,NV;Wallock,L;Kelley,MR
乙醇（EtOH）对雄性啮齿动物生殖的影响已被充分表征为促黄体生成激素（LH），并报告了抑制垂体释放LH的情况。我们以前曾报道，体内急性乙醇（EtOH）暴露导致β-LH基因表达和垂体蛋白质释放的快速和显著抑制。这种β-LH基因表达的抑制并不伴随着共同α-亚基mRNA的变化。为了进一步探讨乙醇对雄性啮齿类动物生殖的影响，我们将研究扩展到促卵泡激素（FSH）、下丘脑促黄体激素释放激素（LHRH）以及垂体蛋白激酶C（PKC）。这些水平在6和24小时恢复到生理盐水注射对照值。尽管血清FSH下降，但在任何时间点垂体内FSH含量均无变化;在血清水平下降的情况下，垂体FSH缺乏提示FSH释放受损。与之前观察到的并在本研究中证实的β-LH稳态mRNA水平下降相反，在任何时间点β-FSH稳态mRNA均未发生变化，表明EtOH对这两种促性腺激素的表达具有二分效应。还评估了PKC水平，发现在任何时间点均不受EtOH影响。这种酶在促性腺激素的跨膜信号传导中很重要，虽然已知EtOH会影响其他细胞中的PKC，但似乎EtOH对促性腺激素的影响并不在此水平上介导。最后，通过放射免疫测定法测定下丘脑促黄体生成素释放激素（LHRH）含量，在任何时间点均未发现该下丘脑肽的变化。我们得出结论，乙醇对垂体促性腺激素基因表达的影响是不均匀的，β-LH选择性抑制而β-FSH不变。这两种促性腺激素的释放似乎受到乙醇的损害，而垂体PKC和下丘脑LHRH含量不变。
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.