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为探索醋氨酚（Ａｃｅ）致大鼠着床前胚泡毒性的机制，大鼠孕后以苯巴比妥（ｐｈｅ）或西咪替丁（Ｃｉｍ）预处理，并于孕ｄ３ｉｇＡｃｅ０．２５，０．５和ｌｇ／ｋｇ（阳性阴道涂片为孕ｄｏ）。ｄ４收集胚泡，观察其细胞数、微核率、有丝分裂指数和胚泡化作用。结果Ｐｈｅ预处理组胚泡微核率和具微核胚泡率显著升高，并与Ａｃｅ呈剂量依赖关系；而用Ｃｉｍ预处理组则呈微核率降低趋势，但胚泡平均细胞数显著减少。以上各组胚泡化作用与溶剂对照组无显著差异。揭示Ａｃｅ对整体大鼠着床前胚泡的细胞毒性主要由其本身引起，而遗传毒性则主要是由其经细胞色素Ｐ４５０氧化产生的代谢物所引起。Ａｃｅ及其代谢物对大鼠着床前胚胎的胚泡化作用均无显著影响。
In order to explore the mechanism of acetaminophen (Ace) induced preimplantation embryogenesis in rats, rats were pretreated with either phenobarbital (phe) or cimetidine (Cim) after pregnancy and d3igAce 0.25, 0.5 and lg / kg (positive vaginal smear for pregnant do). D4 blastocyst collection, observed the number of cells, micronucleus rate, mitotic index and blastocyst. Results The numbers of blastocyst micronuclei and blastocyst were significantly increased in Phe pretreatment group and were in a dose-dependent manner with Ace. However, the pretreatment with Pim showed a tendency of decreasing the micronucleus rate, but the average blastocyst number was significantly cut back. The above groups of blastocyst and solvent control group no significant difference. Revealed that cytotoxicity of Ace on preimplantation blastocysts of whole rats mainly caused by itself, while genotoxicity was mainly caused by its metabolites produced by the oxidation of cytochrome P450. Ace and its metabolites had no significant effect on the blastocystization of preimplantation embryos in rats.