Anderson R A, Reddy J M, Joyce C, Willis B R, Van der Ven H, Zaneveld L J
Biol Reprod. 1982 Nov;27(4):833-40. doi: 10.1095/biolreprod27.4.833.
Ethanol reduced the in vitro fertilizing capacity of mouse spermatozoa in a dose-dependent manner, at concentrations commonly observed after ethanol ingestion by man and experimental animals (100-400 mg%). At these ethanol levels, sperm motility and the integrity and fertilizing capacity of the oocyte were not affected, nor was parthenogenic cleavage induced. Data indicated that ethanol prevents the capacitation of the spermatozoa. Its inhibitory effect could be reversed by incubation of the alcohol-treated spermatozoa in alcohol-free capacitation medium. At similar concentrations, t-butanol had no effect on fertilization, suggesting that inhibition by ethanol is mediated by a mechanism other than a "solvent" effect. Although the alcohol dehydrogenase inhibitor, pyrazole, prevented the inhibition of fertilization by ethanol, acetaldehyde (the product of ethanol oxidation) was without effect. These data indicate that the inhibition of capacitation by ethanol is mediated via its metabolism by spermatozoa but not by the immediate product of ethanol oxidation.
乙醇以剂量依赖方式降低了小鼠精子的体外受精能力，其浓度与人类和实验动物摄入乙醇后常见的浓度（100 - 400毫克%）相当。在这些乙醇水平下，精子活力、卵母细胞的完整性和受精能力均未受到影响，孤雌生殖分裂也未被诱导。数据表明乙醇可阻止精子获能。通过将经酒精处理的精子在无酒精的获能培养基中孵育，其抑制作用可被逆转。在相似浓度下，叔丁醇对受精无影响，这表明乙醇的抑制作用是由“溶剂”效应以外的机制介导的。虽然酒精脱氢酶抑制剂吡唑可阻止乙醇对受精的抑制作用，但乙醛（乙醇氧化产物）却无此作用。这些数据表明，乙醇对获能的抑制作用是通过精子对其代谢介导的，而非由乙醇氧化的直接产物介导。
