Laboratorio de Reproducción y Fisiopatología Materno-Embrionaria, Instituto de Fisiología, Biología Molecular y Neurociencias, Departamento de Biodiversidad y Biología Experimental, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Argentina.
Cell Biol Toxicol. 2011 Aug;27(4):237-48. doi: 10.1007/s10565-011-9185-7. Epub 2011 Feb 18.
Since genetic damage induced by ethanol exposure is controversial and incomplete and because germ and somatic cells constitute bioindicators for monitoring reproductive toxicity and genotoxic actions of ethanol consumption, the purpose of the present investigation was to evaluate morphological sperm, oocyte alterations and parental genotoxic effects after sub-chronic ethanol intake in the CF-1 outbred mouse strain. Ethanol 10% was administered to CF-1 adult male (treated males, TM) and female (treated females, TF) mice for 27 days, whereas water was given to controls from both sexes too (CM and CF). Post-treatment micronucleus frequency (MN-PCE/1,000/mouse) and gamete morphology were evaluated. To test whether change of female reproductive status results in maternal genotoxicity, CF-1 females received ethanol 10% (exposed group, periconceptionally treated females (PTF)) or water (control group, pregnant control females (PCF)) in drinking water for 17 days previous and up to 10 days of gestation. TM had a high percentage of abnormal spermatozoa vs CM (p < 0.001) and elevated parthenogenetic activated oocyte frequency appeared in TF vs CF (p < 0.001). Sub-chronic ethanol ingestion induced increased MN frequency in TM and TF (p < 0.01). In PTF, where blood alcohol concentrations were between 19-28 mg/dl, very significantly increased MN frequency was found vs PCF (p < 0.01), whereas MN values were similar to TF. These results show that sub-chronic alcohol ingestion in CF-1 mice produces sperm head dysmorphogenesis and oocyte nuclear anomalies, suggesting that morphological abnormalities in germ cells are probably related to parental genotoxicity after ethanol consumption.
由于乙醇暴露引起的遗传损伤存在争议且不完整，并且生殖细胞和体细胞构成了监测乙醇消费的生殖毒性和遗传毒性作用的生物标志物，因此本研究的目的是评估 CF-1 近交系小鼠亚慢性乙醇摄入后精子、卵子形态改变和亲代遗传毒性作用。10%的乙醇给予 CF-1 成年雄性（处理雄性，TM）和雌性（处理雌性，TF）小鼠，27 天，而水给予来自两个性别的对照（CM 和 CF）。评估处理后微核频率（MN-PCE/1000/只）和配子形态。为了测试雌性生殖状态的变化是否导致母体遗传毒性，CF-1 雌性在饮用水中接受 10%的乙醇（暴露组，围孕期处理的雌性（PTF））或水（对照组，怀孕对照雌性（PCF））17 天，直至妊娠 10 天。TM 的异常精子百分比明显高于 CM（p <0.001），TF 的卵母细胞异常比例明显高于 CF（p <0.001）。亚慢性乙醇摄入导致 TM 和 TF 的 MN 频率增加（p <0.01）。在 PTF 中，血液中的酒精浓度在 19-28mg/dl 之间，与 PCF 相比，MN 频率非常显著增加（p <0.01），而 MN 值与 TF 相似。这些结果表明，CF-1 小鼠的亚慢性酒精摄入导致精子头部畸形和卵母细胞核异常，提示生殖细胞的形态异常可能与乙醇摄入后的亲代遗传毒性有关。
