Ethanol-induced male infertility: impairment of spermatozoa.

Ethanol-induced male infertility: impairment of spermatozoa.
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乙醇引起的男性不育:精子受损。

DOI:
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发表时间:
1983
影响因子:
3.5
通讯作者:
L. Zaneveld
L. Zaneveld
中科院分区:
医学2区
文献类型:
--
作者:
R. Anderson;B. R. Willis;C. Oswald;L. Zaneveld

文献摘要

被引文献

相似文献

乙醇通常被认为是一种生殖毒素。然而,乙醇诱导不孕的机制仍然知之甚少。由于男性生育力取决于精子使卵子受精的能力,因此本研究的目的是检查长期乙醇处理对与精子生育力相关的几个参数的影响。向已证实生育力的雄性C57 Bl/6 J小鼠施用如下液体饮食:5%(v/v)乙醇,持续1)5周; 2)10周; 3)20周;或4)6%(v/v)乙醇,持续5周。每次给药后,评价附睾精子的数量、活力、形态和受精能力。注意到对精子含量的双相效应:用5%乙醇处理5周和10周,精子含量分别增加80%和65%,而用5%乙醇处理20周和用6%乙醇处理5周,精子含量分别减少52%和71%。虽然运动精子的比例不受乙醇的影响,平均前进速度降低,效果取决于乙醇剂量和暴露时间。同样,异常精子的频率也增加了;用5%乙醇处理20周和用6%乙醇处理5周,精子形态异常的频率分别增加了50%和40%。精子的生育力作为乙醇剂量和暴露时间的函数而降低。用5%乙醇处理20周和用6%乙醇处理5周后,精子与小鼠卵子体外受精的能力分别降低了34%(P <0.02)和62%(P <0.001)。已经开发了描述乙醇诱导的雄性不育的动物模型。生殖损害的程度随着摄入乙醇的量和乙醇暴露的持续时间而变化。连续的影响,应该有可能评估男性不育的假定机制造成的慢性乙醇消费。
Ethanol is generally regarded as a reproductive toxin. However, the mechanism(s) of ethanol-induced infertility remain poorly understood. As male fertility depends upon the ability of spermatozoa to fertilize ova, it was the purpose of the present study to examine the effects of chronic ethanol treatment on several parameters related to sperm fertility. Male C57Bl/6J mice of proven fertility were administered liquid diets as follows: 5% (v/v) ethanol for either 1) 5 weeks; 2) 10 weeks; 3) 20 weeks; or 4) 6% (v/v) ethanol for 5 weeks. After each treatment, epididymal spermatozoa were evaluated with respect to quantity, motility, morphology and the ability to fertilize. A biphasic effect on sperm content was noted: 5- and 10-week treatments with 5% ethanol increased content by 80 and 65%, respectively, whereas 20-week treatment with 5% ethanol and 5-week treatment with 6% ethanol decreased content by 52 and 71%, respectively. Although the proportion of motile spermatozoa was unaffected by ethanol, average forward progression velocity was reduced, the effect being dependent on ethanol dose and duration of exposure. Similarly, the frequency of abnormal spermatozoa was increased; 20-week treatment with 5% ethanol and 5-week treatment with 6% ethanol increased the frequency of sperm morphological anomalies by 50 and 40%, respectively. Fertility of spermatozoa was reduced as a function of ethanol dose and duration of exposure. The ability of sperm to fertilize mouse ova in vitro was reduced by 34% (P less than .02) and 62% (P less than .001) subsequent to 20-week treatment with 5% ethanol and 5-week treatment with 6% ethanol, respectively. An animal model has been developed which describes ethanol-induced male infertility. The degree of reproductive impairment varies with the amount of ethanol ingested, and the duration of ethanol exposure. The continuum of effects should make possible the evaluation of putative mechanisms of male sterility resulting from chronic ethanol consumption.