CONICET | Buscador de Institutos y Recursos Humanos

Updated epidemiological studies established a positive correlation between the exposure to environmental particulate matter and increased cardiovascular morbidity and mortality rates. A systemic inflammatory response is known to be triggered after the inhalation of polluted air, which could alter cardiac function, leading to the observed adverse health effects. An imbalance of the oxidative metabolism was proposed to be one of the underlying mechanisms. Hence, the aim of this work was to evaluate this hypothesis in an in vivo acute model of exposure to residual oil fly ashes (ROFA). Female Swiss mice weighting 25 g were treated with a ROFA suspension (1.0 mg/kg) by intranasal instillation. Measurements were made after 3 h. Oxygen consumption by tissue cubes was found to be reversibly decreased by 38% (sham: 1170 ± 40 ng-at O/min g tissue, p < 0.001). Moreover, a 25% significant decrease was observed in respiratory chain complex II activity (sham: 87 ± 5 nmol/min mg prot, p < 0.01), while complex I and IV were not modified (sham: 310 ± 10 nmol/min mg prot and 24 ± 2 min-1 mg prot, respectively). Interestingly, using succinate as substrate, mitochondrial oxygen consumption was significantly decreased by 30% in state 4 respiration (sham: 87 ± 5 ng-at O/min mg prot, p < 0.01) and by 24% in state 3 respiration (sham: 240 ± 20 ng-at O/min mg prot, p < 0.05). However, respiratory control ratios remained unchanged after the treatment (sham: 2.52 ± 0.07). These data indicate that after the exposure to ROFA, respiratory chain complex II activity is decreased in mice heart, contributing to the observed diminished tissue and mitochondrial oxygen consumption, in rest state as well as in active respiration. Supported by: University of Buenos Aires (B107), CONICET (PIP 231), FONCYT (PICT-2008-2574)