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流行病学调查表明镉(Cd)可致前列腺癌。动物实验证实Cd可致睾丸间质细胞瘤。但其致癌机理不清楚。有人认为Cd造成血管损伤引起局部缺血。缺血部位组织产生大量活性氧。推测活性氧在致癌过程的启动和促进阶段起着重要作用。为了探讨Cd的致癌机理。本研究选择雄性Wistar大鼠、体重170～300g,随机分为对照组,Cd非致癌剂量组(4.0μmol/kg,NCD组)和Cd致癌剂量组(30μmol/kg,CD组),分别于注射后6、9和12h,3周,3,6和12个月处死,观察睾丸病理形态学改变。
Epidemiological studies have shown that cadmium (Cd) can cause prostate cancer. Animal experiments confirmed that Cd can cause testicular stromal tumor. But its carcinogenic mechanism is not clear. Some people think that Cd causes vascular damage caused by ischemia. Ischemic tissue produces a large number of reactive oxygen species. Speculated that reactive oxygen species in the carcinogenic process of the start-up and promotion phase plays an important role. In order to investigate the carcinogenic mechanism of Cd. In this study, male Wistar rats weighing 170-300 g were randomly divided into control group, Cd non-carcinogenic dose group (4.0μmol / kg, NCD group) and Cd carcinogenic dose group (30μmol / kg, CD group) After 6, 9 and 12h, 3 weeks, 3,6 and 12 months after sacrifice, pathological changes of testis were observed.