4.1 Article

Environmental polycyclic aromatic hydrocarbon (PAH) exposure and DNA damage in Mexican children

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ELSEVIER
DOI: 10.1016/j.mrgentox.2011.12.006

关键词

PAH metabolism; 1-Hydroxypyrene; DNA damage; Environmental exposures; Genetic polymorphisms

资金

  1. CONACYT-Mexico [87234]

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Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous pollutants presenting a public health risk, particularly to children, a vulnerable population. PAHs have genotoxic and carcinogenic properties, which depend on their metabolism. Many enzymes involved in PAN metabolism, including CYP1A1, CYP1B1, GSTM and GSTT are polymorphic, which may modulate the activation/deactivation of these compounds. We evaluated PAN exposure and DNA damage in children living in the vicinity of the main petrochemical complex located in the Gulf of Mexico, and explored the modulation by genetic polymorphisms of PAH excretion and related DNA damage. The participants (n = 82) were children aged 6-10y attending schools near the industrial area. Urinary 1-hydroxypyrene (1-OHP; a biomarker of PAH exposure) was determined by reverse-phase-HPLC; DNA damage by the comet assay (Olive Tail Moment (OTM) parameter); CYP1A1 *2C and CYP1B1 *3 polymorphisms by real time-PCR; and GSTM1 *0 and GSTT1*0 by multiplex PCR. The median value of 1-OHP was 0.37 mu mol/mol creatinine; 59% of children had higher 1-OHP concentrations than those reported in environmentally exposed adults (0.24 mu mol/mol creatinine). A stratified analysis showed increased DNA damage in children with 1-0HP concentrations greater than the median value. We observed higher 1-OHP concentrations in children with CYP1A1*2C or GSTM1*0 polymorphisms, and a positive influence of CYPIA1 *2C on OTM values in children with the highest PAN exposure. The data indicate that children living in the surroundings of petrochemical industrial areas are exposed to high PAH levels, contributing to DNA damage and suggesting an increased health risk; furthermore, data suggest that polymorphisms affecting activation enzymes may modulate PAN metabolism and toxicity. (C) 2012 Elsevier B.V. All rights reserved.

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