Formaldehyde induces lung inflammation by an oxidant and antioxidant enzymes mediated mechanism in the lung tissue

Autor(es)

Lino-dos-Santos-Franco, Adriana ; Correa-Costa, Matheus ^[1] ; Cardoso dos Santos Durao, Ana Carolina ^[2] ; Ligeiro de Oliveira, Ana Paula ^[1] ; Breithaupt-Faloppa, Ana Cristina ; Bertoni, Jonatas de Almeida ; Oliveira-Filho, Ricardo Martins ; Saraiva Camara, Niels Olsen ^[1] ; Marcourakis, Tania ^[2] ; Tavares-de-Lima, Wothan ^[3]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Inst Biomed Sci, Dept Immunol, BR-05508900 Sao Paulo - Brazil

^[2] Univ Sao Paulo, Fac Pharmaceut Sci, Dept Clin & Toxicol Anal, BR-05508900 Sao Paulo - Brazil

^[3] Univ Sao Paulo, Inst Biomed Sci, Lab Fisiopatol Inflamacao Expt, Dept Pharmacol, BR-05508900 Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Toxicology Letters; v. 207, n. 3, p. 278-285, DEC 15 2011.
• Citações Web of Science: 36

Resumo

Formaldehyde (FA) is an indoor and outdoor pollutant widely used by many industries, and its exposure is associated with inflammation and oxidative stress in the airways. Our previous studies have demonstrated the role of reactive oxygen species (ROS) in lung inflammation induced by FA inhalation but did not identify source of the ROS. In the present study, we investigate the effects of FA on the activities and gene expression of glutathione peroxidase (GPX), glutathione reductase (GR), glutathione S-transferase (GST), superoxide dismutase (SOD) 1 and 2, catalase (CAT), nitric oxide synthase (iNOS and cNOS) and cyclooxygenase (COX) I and 2. The hypothesized link between NADPH-oxidase, nitric oxide synthase and cyclooxygenase, the lung inflammation after FA inhalation was also investigated. For experiments, male Wistar rats were submitted to FA inhalation (1%, 90 min daily) for 3 consecutive days. The treatments with apocynin and indomethacin before the FA exposure reduced the number of neutrophils recruited into the lung. Moreover, the treatments with apocynin and indomethacin blunted the effect of FA on the generation of IL-1 beta, while the treatments with L-NAME and apocynin reduced the generation of IL-6 by lung explants when compared to the untreated group. FA inhalation increased the levels of NO and hydrogen peroxide by BAL cells cultured and the treatments with apocynin and L-NAME reduced these generations. FA inhalation did not modify the activities of GPX, GR, GST and CAT but reduced the activity of SOD when compared to the naive group. Significant increases in SOD-1 and -2, CAT, iNOS, cNOS and COX-1 expression were observed in the FA group compared to the naive group. The treatments with apocynin, indomethacin and L-NAME reduced the gene expression of antioxidant and oxidant enzymes. In conclusion, our results indicate that FA causes a disruption of the physiological balance between oxidant and antioxidant enzymes in lung tissue, most likely favoring the oxidant pathways and thus positively modulating lung inflammation. (C) 2011 Elsevier Ireland Ltd. All rights reserved. (AU)

• Processo FAPESP: 08/50766-1 - Repercussao pulmonar e sistemica apos exposicao de ratos ao formaldeido: papel regulador das especies reativas derivadas do oxigenio e do nitrogenio.
• Beneficiário: Adriana Lino dos Santos Franco
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado