CONICET | Buscador de Institutos y Recursos Humanos

Reactive O2 species production triggered by particulate matter (PM) exposure is able to initiate oxidativedamage mechanisms, which are postulated as responsible for increased morbidity along with the aggravationof respiratory diseases. The aim of this work was to quantitatively analyse the major sources of reactive O2species involved in lung O2 metabolism after an acute exposure to Residual Oil Fly Ashes (ROFAs). Micewere intranasally instilled with a ROFA suspension (1.0 mg/kg body weight), and lung samples wereanalysed 1 h after instillation. Tissue O2 consumption and NADPH oxidase (Nox) activity were evaluated intissue homogenates. Mitochondrial respiration, respiratory chain complexes activity, H2O2 and ATP productionrates, mitochondrial membrane potential and oxidative damage markers were assessed in isolated mitochondria.ROFA exposure was found to be associated with 61% increased tissue O2 consumption, a 30%increase in Nox activity, a 33% increased state 3 mitochondrial O2 consumption and a mitochondrial complexII activity increased by 25%. During mitochondrial active respiration, mitochondrial depolarization and a 53%decreased ATP production rate were observed. Neither changes in H2O2 production rate, nor oxidative damagein isolated mitochondria were observed after the instillation. After an acute ROFA exposure, increasedtissue O2 consumption may account for an augmented Nox activity, causing an increased O2 ?− production.The mitochondrial function modifications found may prevent oxidative damage within the organelle. Thesefindings provide new insights to the understanding of the mechanisms involving reactive O2 species productionin the lung triggered by ROFA exposure.