Contents lists available at ScienceDirect Ecotoxicology and Environmental Safety journal homepage: www.elsevier.com/locate/ecoenv Obese rats are more vulnerable to inflammation, genotoxicity and oxidative stress induced by coal dust inhalation than non-obese rats Juciano Gasparotto a, ⁎ ,1 , Paloma Rodrigues Chaves a,1 , Kátia da Boit Martinello c , Helen Tais da Rosa-Siva a , Rafael Calixto Bortolin c , Luis Felipe Oliveira Silva c , Thallita Kelly Rabelo d , Juliana da Silva b , Fernanda Rabaioli da Silva e , Adriane Perachi Nordin b,e , Karina Soares e , Malu Siqueira Borges e , Daniel Pens Gelain a , José Claudio Fonseca Moreira a a Centro de Estudos em Estresse Oxidativo, Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil b Laboratório de Genética Toxicológica. PPGBIOSAÚDE & PPGGTA-MP, Universidade Luterana do Brasil (ULBRA), Canoas, RS, Brazil c Laboratorio de Toxicología Ambiental - Departamento de Ingeniería Civil y Ambiental – Universidad de la Costa, Calle 58 #55-66, CP 080002 Barranquilla, Atlántico, Colombia d Laboratório de Neurociências e Ensaios Farmacológicos, Departamento de Fisiologia, Universidade Federal de Sergipe, São Cristóvão, SE, Brazil e Laboratório de Biologia Celular e Molecular, Universidade La Salle, Canoas, RS, Brazil ARTICLE INFO Keywords: Coal Inhalation Obesity Oxidative stress Inflammation ABSTRACT Obesity is an important nutritional disorder worldwide. Its association with environmental pollution may trigger an increase in oxidative stress and inflammatory parameters. Coal is a resource used throughout the world as an important fuel source for generating electricity. The ashes released by the coal combustion cause serious pro- blems for human health due to their high toxicity and their capacity to bioaccumulate. The aim of this work was to investigate the effects of coal dust inhalation in the organs of obese and non-obese Wistar rats. Pro-in- flammatory cytokines, oxidative stress, oxidative damage, histological analysis, comet assay, and micronuclei were investigated. Both obesity and coal dust inhalation increased the pro-inflammatory cytokines IL-1β and TNF-α and decreased HSP70 levels in serum, however, in obese animals that inhaled coal dust these changes were more pronounced. Liver histological analysis showed severe microvesicular steatosis in obese animals that inhaled coal dust. Lung histologic investigation showed abnormalities in lung structure of animals exposed to coal dust and showed severe lung distensibility in obese animals exposed to coal dust. The comet assay showed DNA damage in animals subjected to coal. In addition, there were modulations in enzymatic activities and damage to protein and lipids. Based on our results, the coal dust inhalation can potentiate the pro-inflammatory profile present in obese rats. We also observed an increase in the protein oxidative damage in obese rats that inhaled coal dust. Taken together, our results suggest that the combination of obesity and coal inhalation in- creased the risks of the development of diseases related to oxidative stress and inflammation. 1. Introduction Obesity is a worldwide disorder and is associated with cardiovas- cular disease, diabetes and cognitive disorders (Rummel et al., 2016). Data from the World Health Organization (WHO, 2005) estimate that by 2025 more than 2.3 billion adults will be overweight and over 700 million, obese. Genetic, environmental and behavioral factors are im- portant contributors to the development of this condition. The causes of the current obesity epidemic are associated with sedentary lifestyles, increased consumption of unhealthy foods and reduced physical ac- tivity (Awada et al., 2013). Obesity is characterized by excessive storage of adipose tissue (Fernández-Sánchez et al., 2011). Adipose tissue acts as an endocrine organ generating a chronic low-grade inflammation and releasing a variety of bioactive adipokines, including leptin and adiponectin, which are implicated in the homeostasis of physiological and pathological processes involving reactive species production (Marseglia et al., 2015). Overproduction of reactive species may result in oxidative stress and https://doi.org/10.1016/j.ecoenv.2018.08.097 Received 13 July 2018; Received in revised form 24 August 2018; Accepted 26 August 2018 ⁎ Correspondence to: Rua Ramiro Barcelos, 2600 – anexo, CEP 90035-003 Porto Alegre, RS, Brazil. 1 Co-first authors. E-mail address: juciano.gasparotto@gmail.com (J. Gasparotto). Ecotoxicology and Environmental Safety 165 (2018) 44–51 0147-6513/ © 2018 Elsevier Inc. All rights reserved. T