Acute Inhalation Exposure to Ultrafine Carbon Black Alters Mitochondrial Substrate Utilization in the Heart

A majority of deaths associated with air pollution are attributed to cardiovascular and heart diseases. Carbon black that represents the carbon core of particulate matter, a major component of air pollution, has been shown to result in cardiac mitochondrial dysfunction. The goal of this study was to identify mechanisms that potentially regulate cardiac mitochondrial function in acute carbon black exposure. Specifically, we examined whether lysine acetylation, a post-translational modification, impacts cardiac mitochondrial function and contributes to mitochondrial dysfunction observed with carbon black exposure. C57BL/6J animals exposed to 10 mg/m³ CB for 3 h resulted in a significant increase in acetylation of fatty acid oxidation proteins-long and short chain acyl-CoA dehydrogenase and hydroxyacyl-CoA dehydrogenase-which correlated with decreased enzymatic activities. Further, a significant decrease in fatty acid import protein carnitine palmitoyl-transferase 1b was observed. An increase in acetylation of electron transport chain complexes I and V along with increased Complex V activity was observed in carbon black exposed animals. This decrease in import and utilization of fatty acid metabolism was counteracted by an increase in protein and activity level of glucose oxidation protein pyruvate dehydrogenase. These findings suggest that acute exposure to carbon black results in a switch in substrate utilization from fatty acids to glucose that in turn feeds the electron transport chain process in the exposed heart. Finally, these findings present the potential role of lysine acetylation mediated regulation of mitochondrial dysfunction in the acute carbon black exposed model.