在环境中或哺乳动物代谢过程中，杜邦草胺（3-(3,4-二氯苯基)-1,1-二甲基脲）主要转化为3-(3,4-二氯苯基)-1-甲基脲（DCPMU）和3,4-二氯苯胺（DCA）。 先前的研究表明，这些物质对Wistar大鼠的膀胱上皮具有毒性，在特定暴露条件下，可引起膀胱上皮细胞的变性、坏死、增生和最终形成肿瘤。然而，与这种化学物毒性相关的作用机制尚未完全理解。在这种背景下，本文的目的是通过现场研究分析这些化学物对膀胱上皮毒性的潜在机制，涉及细胞死亡和线粒体功能障碍的可能角色。因此，将人1T1膀胱上皮细胞暴露于6个不同浓度的杜邦草胺、DCA和DCPMU，浓度范围为0.5至500μM。结果显示，被测试的化学物诱导了氧化应激和线粒体损伤、细胞周期不稳定和细胞死亡，这些现象在代谢物浓度更高时更为明显。这些数据证实了该实验室以前的研究，并综合表明线粒体功能障碍是引发膀胱上皮细胞变性和死亡的初始事件。

In the environment, or during mammalian metabolism, the diuron herbicide (3-(3,4-dichlorophenyl)-1,1-dimethylurea) is transformed mainly into 3-(3,4-dichlorophenyl)-1-methylurea (DCPMU) and 3,4-dichloroaniline (DCA). Previous research suggests that such substances are toxic to the urothelium of Wistar rats where, under specific exposure conditions, they may induce urothelial cell degeneration, necrosis, hyperplasia, and eventually tumors. However, the intimate mechanisms of action associated with such chemical toxicity are not fully understood. In this context, the purpose of the current in vitro study was to analyze the underlying mechanisms involved in the urothelial toxicity of those chemicals, addressing cell death and the possible role of mitochondrial dysfunction. Thus, human 1T1 urothelial cells were exposed to six different concentrations of diuron, DCA, and DCPMU, ranging from 0.5 to 500 µM. The results showed that tested chemicals induced oxidative stress and mitochondrial damage, cell cycle instability, and cell death, which were more expressive at the higher concentrations of the metabolites. These data corroborate previous studies from this laboratory and, collectively, suggest mitochondrial dysfunction as an initiating event triggering urothelial cell degeneration and death.