DNA repair and metabolic gene polymorphisms affect genetic damage due to diesel engine exhaust exposure

Diesel engine exhaust (DEE) is a complex mixture of toxic gases, halogenated aromatic hydrocarbons, alkyl polycyclic aromatic hydrocarbons, polycyclic aromatic hydrocarbons, benzene derivatives, metals and diesel exhaust particles (DEPs) generated from the incomplete combustion of diesel fuel. Many...

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Autores:
León-Mejía, Grethel
Quintana-Sosa, Milton
de Moya Hernandez, Yurina
Luna Rodríguez, Ibeth
Trindade, Cristiano
Anaya Romero, Marco
Luna-Carrasca, Jaime
Oliveros Ortíz, Ludis
Acosta-Hoyos, Antonio
Ruiz-Benitez, Martha
Franco Valencia, Karen
Rohr, Paula
da Silva, Juliana
Pêgas Henriques, João Antônio
Tipo de recurso:
Fecha de publicación:
2020
Institución:
Universidad Simón Bolívar
Repositorio:
Repositorio Digital USB
Idioma:
OAI Identifier:
oai:bonga.unisimon.edu.co:20.500.12442/5090
Acceso en línea:
https://hdl.handle.net/20.500.12442/5090
Palabra clave:
Diesel exhaust particles
Polymorphism
DNA repair
DNA oxidative damage
Mechanics
Rights
License
Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Description
Summary:Diesel engine exhaust (DEE) is a complex mixture of toxic gases, halogenated aromatic hydrocarbons, alkyl polycyclic aromatic hydrocarbons, polycyclic aromatic hydrocarbons, benzene derivatives, metals and diesel exhaust particles (DEPs) generated from the incomplete combustion of diesel fuel. Many of the compounds in this mixture can cause oxidative damage to DNA and are considered carcinogenic for humans. Further, chronic DEE exposure increases risks of cardiovascular and pulmonary diseases. Despite these pervasive health risks, there is limited and inconsistent information regarding genetic factors conferring susceptibility or resistance to DEE genotoxicity. The present study evaluated the effects of polymorphisms in two base excision repair (BER) genes (OGG1 Ser326Cys and XRCC1 Arg280His), one homologous recombination (HRR) gene (XRCC3 Thr241Met) and two xenobiotic metabolism genes (GSTM1 and GSTT1) on the genotoxicity profiles among 123 mechanics exposed to workplace DEE. Polymorphisms were determined by PCR-RFLP. In comet assay, individuals with the GSTT1 null genotype demonstrated significantly greater % tail DNA in lymphocytes than those with non-null genotype. In contrast, these null individuals exhibited significantly lower frequencies of binucleated (BN) cells and nuclear buds (NBUDs) in buccal cells than non-null individuals. Heterozygous hOGG1 326 individuals (hOGG1 326 Ser/Cys) exhibited higher buccal cell NBUD frequency than hOGG1 326 Ser/Ser individuals. Individuals carrying the XRCC3 241 Met/Met polymorphism also showed significantly higher buccal cell NBUD frequencies than those carrying the XRCC3 241 Thr/Thr polymorphism. We found a high flow of particulate matter with a diameter of < 2.5 μm (PM2.5) in the workplace. The most abundant metals in DEPs were iron, copper, silicon and manganese as detected by transmission electron microscopy–energy-dispersive X-ray spectroscopy (TEM-EDX). Scanning electron microscopy (SEM-EDS) revealed particles with diameters smaller than PM2.5, including nanoparticles forming aggregates and agglomerates. Our results demonstrate the genotoxic effects of DEE and the critical influence of genetic susceptibility conferred by DNA repair and metabolic gene polymorphisms that shed light into the understanding of underlying mechanisms.