INDUCTION OF 8-HYDROXY-2-DEOXYGUANOSINE AND SINGLE-STRAND BREAKS IN DNA OF V79 CELLS BY TETRACHLORO-P-HYDROQUINONE

被引：32

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：

MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS | 1995年 / 329卷 / 01期

关键词：

PENTACHLOROPHENOL; TETRACHLOROHYDROQUINONE; OXIDATIVE DNA DAMAGE; 8-HYDROXY-2'-DEOXYGUANOSINE; V79; CELLS;

D O I：

10.1016/0027-5107(95)00014-A

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

The biocide pentachlorophenol (PCP) is in part metabolized, by microsomal enzymes, to tetrachloro-p-hydroquinone (TCHQ), which easily oxidizes to its semiquinone radical. Redox cycling of this compound produces reactive oxygen species (ROS) which ultimately may damage cellular DNA. Here, we report on DNA damage generated by TCHQ in hamster lung fibroblasts (V79 cells) using 8-hydroxy-2-deoxyguanosine (8-OH-dG) as a marker of a major oxidative genetic lesion and measuring the induction of DNA single-strand breaks (DNA SSB) with the aid of the alkaline elution assay. TCHQ was administered to cell cultures in concentrations of 6.25, 12.5, 25, and 50 mu M for 1 h. 6.25 and 12.5 mu M had no significant effect on both parameters, whereas the higher concentrations resulted in increases of the level of 8-OH-dG (2.3- and 2.0-fold, respectively) and induced DNA SSB. The latter lesion may arise. from (i) direct attack of OH, (ii) repair of hydroxylated DNA bases, or (iii) cytotoxic effects. Metabolic transformation of PCP to TCHQ and/or other metabolites with quinoid structures and the subsequent generation of ROS, producing oxidative DNA damage, may play a role in PCP-induced carcinogenicity observed in mice.

引用

页码：29 / 36

页数：8

共 42 条

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