中文摘要：

目的探讨二乙基己基邻苯二甲酸（DEHP）对附睾生殖功能的损害和可能机制，探寻DEHP毒性作用的拮抗剂。方法出生后20d（PND20）和50d（PND50）雄性KM小鼠分别随机分为正常对照组、玉米油组、DEHP组和DEHP＋葡萄糖酸锌组，连续灌胃10d，观察各期各组小鼠附睾组织学改变，检测雄激素受体（AR）、雌激素受体（ER）表达水平；体外培养PND20和PND50小鼠附睾上皮细胞，MTT法测定附睾上皮细胞活性，测定唾液酸（SA）含量、α-1，4-糖苷酶活性及乳酸脱氢酶（LDH）活力。结果体内实验表明DEHP可导致附睾萎缩等组织病理学改变，并可导致附睾组织AR水平上调和ER水平下调（P〈0．01）；体外实验表明DEHP可导致附睾上皮细胞活性降低，而DEHP＋葡萄糖酸锌组附睾的形态、结构及功能均未见明显改变。结论DEHP可使附睾的结构和功能受损，锌对DEHP所致附睾生殖毒性具有拮抗作用。

英文摘要：

Objective To study reproductive functional lesions of Di（2-ethylhexyl） Phthalate （DEHP） on epididymis, and to find antagon which can repress the toxicity. Methods In vivo study, postnatal day 20 （PND20） and PND50 male KM mice were randomly divided into normal control, corn oil, DEHP and DEHP ＋ Zinc gluconate group. In each stage and group, after been gavaged for 10 days, epididymal histopathologic changes and androgen receptor （AIR） and estrogen receptor （ER） in epididymis were detected. In vitro study, epididymal epithelial cells of PND20 and PND50 mice were cultured. Viability of epididymal epithelial cells were measured using MTT assay, content of sialic acid （SA） and the activity of α-1,4-glucosidase and lactic acid dehydrogenase （LDH） were investigated. Results DEHP induced epididymis atrophy and conspicuous histopathologic ultrastructure changes, upregulated AIR and down-regulated ER. No conspicuous variations were found in DEHP ＋ Zinc gluconate group. Conclusions DEHP can induce lesions of epididymal structure and function. Zinc is an antagon to DEHP toxicity.