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Pulmonary Exposure to Combustion Particulate Matter Induces Myocardial Mitochondrial injury and impaired tolerance to ischemia reoxygenation
Citation:
Golomb, E., D. Matza, C. Cummings, H. Schwalb, U. P. KODAVANTI, A. Schneider, E. Houminer, A. Korach, A. Nyska, AND O. M. Shapira. Pulmonary Exposure to Combustion Particulate Matter Induces Myocardial Mitochondrial injury and impaired tolerance to ischemia reoxygenation. Presented at International Society for Heart Research, Haifa, ISRAEL, June 26 - 29, 2011.
Impact/Purpose:
This study shows that vanadium containing particulate matter induces cardiac cell injury and mitochondrial ultrastructural alterations under ischemic condition 48 hours after a single intratracheal exposure in rats.
Description:
Background and aim: Air pollution is associated with increased morbidity and mortality of acute and chronic coronary heart disease. This effect has been attributed to oxidative stress, thrombogenesis, elevation of blood pressure, inflammation and accelerated atherosclerosis. Herein, we aimed to assess the effect of pulmonary exposure to vanadium-rich respirable fraction of oil combustion particulate matter (PM; HP-10) on the intrinsic myocardial ischemic tolerance and mitochondrial integrity in rats. Methods: Healthy male Sprague-Dawley rats, weighing 300±20g, received a single intratracheal instillation of saline (control), 0.5mg/Kg or 2.5 mg/Kg of HP-10. Their hearts were studied 48h later by the MTT colorimetric assay and by electron microscopy. Results: Isolated heart slices of rats exposed to PM exhibited no apparent inhibition of mitochondrial dehydrogenase activity in oxygenated conditions, as determined by the MTT assay. However, in conditions of simulated ischemia / reoxygenation these heart slices showed a consistent and significant decrease in dehydrogenase activity by ~30% compared to controls. PM caused a significant myocardial mitochondrial injury, consisting of swelling, fusion and fissures of the internal membrane. Conclusion: Instillation of vanadium-rich PM in rats causes a myocardial mitochondrial injury, reflected by decreased ischemic tolerance. (These views do not represent US EPA policy).