Ethanol-induced male reproductive tract pathology as a function of ethanol dose and duration of exposure.
Ethanol-induced male reproductive tract pathology as a function of ethanol dose and duration of exposure.
复制标题
乙醇引起的男性生殖道病理学是乙醇剂量和暴露持续时间的函数。
DOI：
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发表时间：
1983
影响因子：
3.5
通讯作者：
L. Zaneveld
中科院分区：
文献类型：
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作者：
B. R. Willis;R. Anderson;C. Oswald;L. Zaneveld
男性长期摄入乙醇会导致生殖功能障碍的几种表现。然而，关于1)在男性生殖道中产生病理变化所必需的乙醇水平或乙醇暴露的持续时间知之甚少；或2)乙醇发挥其毒性作用的机制。本研究的目的是建立一种动物模型来描述乙醇引起的雄性生殖衰竭，并确定乙醇暴露会改变男性生殖道功能的条件。经证实的繁殖雄性C57Bl/6J小鼠分别饲喂5% （v/v）乙醇液体饲料5周、10周或20周，或饲喂6% （v/v）乙醇饲料5周。在食用5%和6%乙醇饲料的动物中，每日血液乙醇水平分别达到125至200毫克和268毫克/100毫升。血浆睾酮水平在所有治疗过程中都有所降低，这种效果似乎是可逆的。治疗期间血浆睾酮与血乙醇水平相关性较差（r = 0.28）。治疗后，生殖道病理包括睾丸和附属性器官重量减少，精子发生减少，未成熟生殖细胞进入精小管腔的脱屑增加，无活性精小管的频率增加。虽然在5%乙醇饮食治疗5周后发现的变化很小，但在更长时间的暴露或相同时间的6%乙醇治疗后，缺陷变得越来越明显。所有治疗方案均未导致肝酶标记物血浆水平的改变或组织学外观的改变。结果表明，男性生殖功能对乙醇剂量和暴露时间均敏感。在本研究中描述的动物模型应该在评估假定的酒精诱导男性生殖功能障碍的机制方面具有实用价值。
Chronic ethanol ingestion by the male results in several manifestations of reproductive dysfunction. However, little is known concerning 1) the level of ethanol or duration of ethanol exposure necessary to produce pathological changes in the male reproductive tract; or 2) mechanism(s) by which ethanol exerts its toxic effects. The purpose of the present study was to develop an animal model which describes ethanol-induced male reproductive failure and to define conditions of ethanol exposure which alter male reproductive tract function. Proven breeder male C57Bl/6J mice were maintained on either a 5% (v/v) ethanol liquid diet for periods of 5, 10 or 20 weeks or a 6% (v/v) ethanol diet for 5 weeks. Daily blood ethanol levels peaked at 125 to 200 and 268 mg/100 ml in animals consuming the 5 and 6% ethanol diets, respectively. Plasma testosterone levels were depressed throughout all treatments, an effect which appeared reversible. Plasma testosterone was poorly correlated (r = 0.28) with blood ethanol levels during treatment. After treatment, reproductive tract pathology included reduced testicular and accessory sex organ weights, decreased spermatogenesis, increased desquamation of immature germ cells into the seminiferous tubule lumina and increased frequency of inactive seminiferous tubules. Whereas minimal changes were noted after 5 weeks treatment with the 5% ethanol diet, deficiencies became increasingly evident after either longer exposure periods or treatment with 6% ethanol for the same period. None of the treatment regimens resulted in altered plasma levels of hepatic enzyme markers or in altered histological appearance. The data indicate that male reproductive function is sensitive to both ethanol dose and duration of exposure. The animal model described in the present study should have utility in the evaluation of putative mechanisms of ethanol-induced male reproductive dysfunction.