DNA repair and metabolic gene polymorphisms affect genetic damage due to diesel engine exhaust exposure
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Fecha
2020-03
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
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Editor
Springer
Resumen
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.
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Palabras clave
Diesel exhaust particles, Polymorphism, DNA repair, DNA oxidative damage, Mechanics