Genotoxic and epigenotoxic effects in mice exposed to concentrated ambient fine particulate matter (PM2.5) from São Paulo city, Brazil
Autor: | Paolo Di Mascio, Antonio Anax Falcão de Oliveira, Michelle Francini Dias, Tiago Franco de Oliveira, Miriam Lemos, Mariana Matera Veras, Marisa Helena Gennari de Medeiros, Paulo Hilário Nascimento Saldiva, Ana Paula de Melo Loureiro, Tania Marcourakis |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Antioxidant Health Toxicology and Mutagenesis medicine.medical_treatment Glutathione reductase lcsh:Industrial hygiene. Industrial welfare 010501 environmental sciences Toxicology medicine.disease_cause 01 natural sciences Superoxide dismutase Andrology 03 medical and health sciences chemistry.chemical_compound lcsh:RA1190-1270 medicine METILAÇÃO DE DNA 0105 earth and related environmental sciences lcsh:Toxicology. Poisons Kidney DNA methylation biology DNA adducts General Medicine Glutathione 030104 developmental biology medicine.anatomical_structure chemistry Apoptosis Oxidative stress biology.protein Particulate matter lcsh:HD7260-7780.8 |
Zdroj: | Particle and Fibre Toxicology, Vol 15, Iss 1, Pp 1-19 (2018) Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual) Universidade de São Paulo (USP) instacron:USP |
ISSN: | 1743-8977 |
DOI: | 10.1186/s12989-018-0276-y |
Popis: | Background The Metropolitan Area of São Paulo has a unique composition of atmospheric pollutants, and positive correlations between exposure and the risk of diseases and mortality have been observed. Here we assessed the effects of ambient fine particulate matter (PM2.5) on genotoxic and global DNA methylation and hydroxymethylation changes, as well as the activities of antioxidant enzymes, in tissues of AJ mice exposed whole body to ambient air enriched in PM2.5, which was concentrated in a chamber near an avenue of intense traffic in São Paulo City, Brazil. Results Mice exposed to concentrated ambient PM2.5 (1 h daily, 3 months) were compared to in situ ambient air exposed mice as the study control. The concentrated PM2.5 exposed group presented increased levels of the oxidized nucleoside 8-oxo-7,8-dihydro-2′-deoxyguanosine in lung and kidney DNA and increased levels of the etheno adducts 1,N 6-etheno-2′-deoxyadenosine and 1,N 2-etheno-2′-deoxyguanosine in kidney and liver DNA, respectively. Apart from the genotoxic effects, the exposure to PM2.5 led to decreased levels of the epigenetic mark 5-hydroxymethylcytosine (5-hmC) in lung and liver DNA. Changes in lung, liver, and erythrocyte antioxidant enzyme activities were also observed. Decreased glutathione reductase and increased superoxide dismutase (SOD) activities were observed in the lungs, while the liver presented increased glutathione S-transferase and decreased SOD activities. An increase in SOD activity was also observed in erythrocytes. These changes are consistent with the induction of local and systemic oxidative stress. Conclusions Mice exposed daily to PM2.5 at a concentration that mimics 24-h exposure to the mean concentration found in ambient air presented, after 3 months, increased levels of DNA lesions related to the occurrence of oxidative stress in the lungs, liver, and kidney, in parallel to decreased global levels of 5-hmC in lung and liver DNA. Genetic and epigenetic alterations induced by pollutants may affect the genes committed to cell cycle control, apoptosis, and cell differentiation, increasing the chance of cancer development, which merits further investigation. |
Databáze: | OpenAIRE |
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