Mitochondrial dysfunction and NADPH oxidase activation after the exposure to residual oil fly ash

EVELSON P; MAGNANI ND; MARCHINI T; VANASCO V; TASAT DR; ALVAREZ S

Buenos Aires

Congreso; VIII International Congress of SFRBM sag; 2013

Society For Free Radicals and Biology south American group

Reactive O2 species production triggered by particulate matter (PM) exposure are able to initiate oxidative damage mechanisms, which are postulated as responsible for increased morbidity along with the aggravation of respiratory diseases. The aim of this work was to analyse the major sources of reactive O2 species involved in lung O2 metabolism after an acute exposure to Residual Oil Fly Ashes (ROFA). Mice were intranasally instilled with a ROFA suspension (1.0 mg/kg body weight), and lung samples were analysed 1 h after instillation. ROFA exposure was found to be associated with 61% increased tissue O2 consumption, a 30% increase in NADPH oxidase (Nox) activity, a 33% increased state 3 mitochondrial O2 consumption and a mitochondrial complex II activity increased by 25%. During mitochondrial active respiration, mitochondrial depolarization and a 53% decreased ATP production rate were observed. No changes were observed in H2O2 production rate, or oxidative damage in isolated mitochondria. After a ROFA exposure, increased tissue O2 consumption may account for an augmented Nox activity and mitochondrial state 3 respiration. The mitochondrial function modifications found may prevent oxidative damage within the organelle. These findings provide new insights to the understanding of the mechanisms involving reactive O2 species production in the lung triggered by ROFA exposure.