Sistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSPDAMIANI, Roberto MarquesPIVA, Marcella OdyPETRY, Marcelo RafaelSALDIVA, Paulo Hilario NascimentoOLIVEIRA, Alexandre Tavares Duarte deRHODEN, Claudia Ramos2013-10-022013-10-022012TOXICOLOGY MECHANISMS AND METHODS, v.22, n.7, p.533-539, 20121537-6516https://observatorio.fm.usp.br/handle/OPI/2573The current study aimed to determine the role of oxidants in cardiac and pulmonary toxicities induced by chronic exposure to ROFA. Eighty Wistar rats were divided into four groups: G1 (10 mu L Saline), G2 (ROFA 50 mu g/10 mu L), G3 (ROFA 250 mu g/10 mu L) and G4 (ROFA 500 mu g/10 mu L). Rats received ROFA by nasotropic instillation for 90 days. After that, they were euthanized and bronchoalveolar lavage (BAL) was performed for total count of leukocytes, protein and lactate dehydrogenase (LDH) determinations. Lungs and heart were removed to measure lipid peroxidation (MDA), catalase (CAT) and superoxide dismutase (SOD) activity. BAL presented an increase in leukocytes count in G4 in comparison to the Saline group (p = 0.019). In lung, MDA level was not modified by ROFA, while CAT was higher in G4 when compared to all other groups (p = 0.013). In heart, G4 presented an increase in MDA (p = 0.016) and CAT (p = 0.027) levels in comparison to G1. The present study demonstrated cardiopulmonary oxidative changes after a chronic ROFA exposure. More specifically, the heart tissue seems to be more susceptible to oxidative effects of long-term exposure to ROFA than the lung.engrestrictedAccessROFAchronic exposureair pollutioncardiopulmonary oxidative stressparticulate air-pollutionconcentrated ambient particlescoronary-heart-diseasealveolar macrophageinhalation exposurelipid-peroxidationhydrogen-peroxidesao-paulopulmonaryinflammationarticleCopyright INFORMA HEALTHCARE10.3109/15376516.2012.692109Toxicology