Dahlhaus M, Almstadt E, Henschke P, Lüttgert S, Appel K E
Division for Plant Protection Products and Pesticides, Federal Institute for Health Protection of Consumers and Veterinary Medicine, Berlin, Germany.
Arch Toxicol. 1996;70(7):457-60. doi: 10.1007/s002040050299.
Incubation of the pentachlorophenol (PCP) metabolites, tetrachloro-p-benzoquinone (chloranil, TCpBQ), tetrachloro-p-hydroquinone (TCpHQ) and tetrachloro-p-benzoquinone (TCoBQ) with V79 Chinese hamster cells led to a significant enhancement of the amount of 8-hydroxydeoxyguanosine (8-OH-dG) in DNA. With PCP itself and the metabolite tetrachloro-o-hydroquinone (TCoHQ) no distinct induction of this lesion could be observed. The average yields of 8-OH-dG were about 2-2.5 times above background levels. In addition, TCpBQ and TCpHQ were able to generate DNA single-strand breaks, while PCP, TCoHQ and TCoBQ failed to induce this lesion. All incubations were performed for 1 h without exogenous metabolic activation and concentrations were 25 microM of the respective agent. It is concluded that these metabolites may contribute to the carcinogenicity of PCP observed in mice, by generating reactive oxygen species (ROS) through their redox cycling properties.
将五氯苯酚（PCP）的代谢产物四氯对苯醌（四氯苯醌，TCpBQ）、四氯对苯二酚（TCpHQ）和四氯邻苯醌（TCoBQ）与V79中国仓鼠细胞一起孵育，导致DNA中8-羟基脱氧鸟苷（8-OH-dG）的量显著增加。对于PCP本身及其代谢产物四氯邻苯二酚（TCoHQ），未观察到这种损伤的明显诱导。8-OH-dG的平均产量比背景水平高出约2至2.5倍。此外，TCpBQ和TCpHQ能够产生DNA单链断裂，而PCP、TCoHQ和TCoBQ未能诱导这种损伤。所有孵育均在无外源性代谢活化的情况下进行1小时，各试剂的浓度为25微摩尔。结论是，这些代谢产物可能通过其氧化还原循环特性产生活性氧（ROS），从而导致在小鼠中观察到的PCP致癌性。
