Steiner J, Kirsteins L, LaPaglia N, Lawrence A, Williams D, Emanuele N, Emanuele M
Department of Medicine, Loyola University of Chicago Stritch School of Medicine, Maywood, IL 60153, USA.
Alcohol. 1997 May-Jun;14(3):209-11. doi: 10.1016/s0741-8329(96)00113-9.
Alterations in the protein kinase C (PKC) pathway may interrupt anterior pituitary luteinizing hormone (LH) synthesis and/or secretion, which may impair normal reproductive function. Work by our laboratory and others has shown that EtOH has profound deleterious effects on the regulation of the hypothalamic-pituitary-gonadal (HPG) axis. The present study focuses on PKC translocation from the cytosol to the membrane of anterior pituitary after acute EtOH exposure. Serum levels of LH were measured at three time points (15, 30, and 90 min) after an IP injection of either saline or 3 g/kg EtOH in adult castrated male rats. LH levels dropped significantly (p < 0.03) in EtOH-injected compared to saline-injected control animals. In the same animals, EtOH significantly suppressed PKC localization at its active site at the pituitary cell membrane (p < 0.05). These findings suggest that the mechanism of EtOH's suppression of LH is mediated, at least in part, through a decrease in PKC translocation to the anterior pituitary cell membrane.
蛋白激酶C(PKC)信号通路的改变可能会干扰垂体前叶促黄体生成素(LH)的合成和/或分泌,进而损害正常的生殖功能。我们实验室及其他研究机构的工作表明,乙醇(EtOH)对下丘脑-垂体-性腺(HPG)轴的调节具有严重的有害影响。本研究聚焦于成年去势雄性大鼠急性暴露于乙醇后,PKC从前垂体细胞质向细胞膜的转位情况。在腹腔注射生理盐水或3 g/kg乙醇后的三个时间点(15、30和90分钟)测量血清LH水平。与注射生理盐水的对照动物相比,注射乙醇的动物LH水平显著下降(p < 0.03)。在同一批动物中,乙醇显著抑制了PKC在垂体细胞膜活性位点的定位(p < 0.05)。这些发现表明,乙醇抑制LH的机制至少部分是通过PKC转位至垂体前叶细胞膜的减少介导的。