取雌性Wistar大鼠从妊娠日起用10、100、500mg/(kg.d)邻苯二甲酸二(2-乙基)己酯(DEHP)连续灌胃染毒至孕19d。测定睾丸脂质过氧化产物丙二醛(MDA)水平,超氧化物歧化酶(SOD)活力,睾丸组织中铜、锌微量元素含量。随着DEHP剂量的增加,500mg/(kg.d)DEHP染毒组子代大鼠睾丸中的MDA含量增加,SOD活力降低,与对照组相比,差异具有统计学意义(P<0.05)。500mg/(kg.d)DEHP染毒组的锌元素含量与对照组相比,显著降低,差异具有统计学意义(P<0.05);而铜含量在各组间差别不明显。提示DEHP胚胎期暴露对子代雄性大鼠的生殖系统发育具有明显的毒性作用,可增加大鼠睾丸组织的脂质过氧化水平,同时会干扰生殖系统锌元素的代谢。这是DEHP致子代雄性大鼠生殖发育毒性的可能机制之一。 Female Wistar rats were dosed with 10,100 and 500 mg / (kg.d) di-2-ethylhexyl phthalate (DEHP) daily until the 19th day of gestation. The contents of malondialdehyde (MDA), superoxide dismutase (SOD) and contents of copper and zinc in testis tissue were determined. With the increase of DEHP dose, the content of MDA in the testis of the offspring of 500mg / (kg.d) DEHP group increased and the activity of SOD decreased. Compared with the control group, the difference was statistically significant (P <0.05). Compared with control group, the content of zinc in DEHP 500 mg / (kg · d) group was significantly lower than that in control group (P <0.05), but the difference of copper content was not significant among the groups. These results suggest that DEHP embryo exposure has obvious toxic effect on the reproductive system of offspring male rats, which can increase the level of lipid peroxidation in rat testis and interfere with the zinc metabolism in the reproductive system. This is one of the possible mechanisms of the reproductive and developmental toxicity of DEHP-induced male rats.