Oxidative DNA lesions in V79 cells mediated by pentachlorophenol metabolites

被引：53

作者：

Dahlhaus, M ^{[1
]}

Almstadt, E ^{[1
]}

Henschke, P ^{[1
]}

Luttgert, S ^{[1
]}

Appel, KE ^{[1
]}

机构：

[1] FED INST HLTH PROTECT CONSUMERS & VET MED, DIV PLANT PROTECT PROD & PESTICIDES, D-14191 BERLIN, GERMANY

来源：

ARCHIVES OF TOXICOLOGY | 1996年 / 70卷 / 07期

关键词：

pentachlorophenol; tetrachloro-p-benzoquinone (chloranil); tetrachloro-p-hydroquinone; tetrachloro-o-benzoquinone; tetrachloro-o-hydroquinone; oxidative DNA damage; 8-hydroxy-2'-deoxyguanosine; V79; cells;

D O I：

10.1007/s002040050299

中图分类号：

R99 [毒物学（毒理学）];

学科分类号：

100405 ;

摘要：

Incubation of the pentachlorophenol (PCP) metabolites, tetrachloro-p-benzoquinone (chloranil, TCpBQ), tetrachloro-p-hydroquinone (TCpHQ) and tetrachloro-o-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. III 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 mu M 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.

引用

页码：457 / 460

页数：4

共 39 条

[1] METABOLISM OF PENTACHLOROPHENOL INVIVO AND INVITRO [J].