The Role of Catechols and Free Radicals in Benzene Toxicity: An Oxidative DNA Damage Pathway

被引：75

作者：

Barreto, George ^{[1
]}

Madureira, Diego ^{[2
]}

Capani, Francisco ^{[3
]}

Aon-Bertolino, Laura ^{[3
]}

Saraceno, Ezequiel ^{[3
]}

Alvarez-Giraldez, Lisandro Diego ^{[2
]}

机构：

[1] CSIC, Inst Cajal, E-28002 Madrid, Spain

[2] Univ Fed Bahia, Lab Neuroquim & Biol Celular, Salvador, BA, Brazil

[3] Univ Buenos Aires, CONICET, Inst Invest Cardiol Prof Dr Alberto C Taquini INI, Dept Neurociencias, Buenos Aires, DF, Argentina

来源：

ENVIRONMENTAL AND MOLECULAR MUTAGENESIS | 2009年 / 50卷 / 09期

关键词：

benzene; catechol; toxicity; reactive oxygen species; DNA damage; EXTENDED-TERM CULTURES; HUMAN-LYMPHOCYTES; STRAND BREAKS; PARKINSONS-DISEASE; LEUKEMIA-CELLS; MITOCHONDRIAL RESPIRATION; GENETIC POLYMORPHISMS; NEUROBLASTOMA-CELLS; REPAIR CAPACITY; OXIDIZED FORM;

D O I：

10.1002/em.20500

中图分类号：

X [环境科学、安全科学];

学科分类号：

08 ; 0830 ;

摘要：

Benzene is a widespread volatile compound and an environmental contaminant. Since it causes important toxic effects in workers exposed to low levels, long-term exposure to this compound has been extensively studied. Leukemia, blood disorders, bone marrow depression, and some types of cancer are directly related to benzene-initiated toxicity. Bioactivation of benzene can lead to the formation of hazardous metabolites such as phenol, hydroquinone, and catechol. Catechol forms semiquinones and reactive quinones that are pre-sumed to play an important role in the generation of reactive oxygen species (ROS). ROS formation can directly induce single and double strand breaks in the DNA, oxidized nucleotides, and hyper-recombination, and consequently produces deleterious genetic changes. In this review, we hove addressed the cytotoxic effects of benzene and its main metabolite, catechol, focusing on the oxidative pathway and further DNA damage. Environ. Mol. Mutagen. 50:771-780, 2009. (C) 2009 Wiley-Liss, Inc.

引用

页码：771 / 780

页数：10

共 114 条

[1] Release of iron from ferritin by metabolites of benzene and superoxide radical generating agents [J].