【摘要】 目的 探讨消毒副产物卤代苯醌的毒理学效应及其潜在作用机制，为后续体内毒性研究提供依据。方法 以人膀胱癌细胞株T24为研究对象，选择代表性卤代苯醌2,6-二氯-1,4-苯醌（DCBQ）进行处理。采用MTS法检测细胞活力，使用2’,7’-二氯荧光素二乙酸酯检测活性氧（ROS）生成水平，并通过氧化DNA损伤ELISA试剂盒测定8-羟基脱氧鸟苷（8-OHdG）含量。结果 DCBQ处理降低了T24细胞的存活率，其24小时IC₅₀值为92.0（95%CI:85.3～98.6） nM。当DCBQ浓度达到50μM以上时，T24细胞内ROS生成增加，且呈浓度依赖性（P<0.05）。与对照组相比，经75μM、100μM及125μM DCBQ处理的细胞中，基因组DNA内8-OHdG水平升高（P<0.05）。结论 DCBQ对T24细胞的毒性作用可能与ROS介导的DNA氧化损伤有关。更多还原

【Abstract】 Objective To explore the toxicological effects and potential mechanisms of disinfection by-product halobenzoquinone,and to provide a basis for subsequent in vivo toxicity studies.Methods Taking the human bladder cancer cell line T24 as study object,which was treated with a representative halobenzoquinone,2,6-dichloro-1,4-benzoquinone（DCBQ）. Cell viability was assessed using the MTS assay. Intracellular reactive oxygen species generation was measured with2’, 7’-dichlorodihydrofluorescein diacetate（ROS）, and oxidative DNA damage was evaluated by quantifying genomic8-hydroxy-2’-deoxyguanosine（8-OHd G） levels using an ELISA kit.Results DCBQ treatment significantly reduced the survival of T24 cells in a concentration-dependent manner, with a 24-hour IC₅₀value of 92.0（95%CI: 85.3-98.6） nM.After treating T24 cells with DCBQ above 50 μM, a significant increase in ROS was observed and the increase was concentration dependent（P<0.05）. Compared with the control group, cells treated with 75 μM, 100 μM and 125 μM DCBQ showed increased levels of 8-OHd G in genomic DNA（P<0.05）.Conclusion These findings suggest that the cytotoxicity of DCBQ in T24 cells may be associated with ROS-induced oxidative DNA damage.更多还原