Mitochondrial Ca2+ flux and respiratory enzyme activity decline are early events in cardiomyocyte response to H2O2

Journal of Molecular and Cellular Cardiology
Xilin LongJosé Marín-García

Abstract

Oxidative stress is involved in mitochondrial apoptosis, and plays a critical role in ischemic heart disease and cardiac failure. Exposure of cardiomyocytes to H(2)O(2) leads to oxidative stress and mitochondrial dysfunction. In this study, we investigated the temporal order of mitochondrial-related events in the neonatal rat cardiomyocyte response to H(2)O(2) treatment. At times ranging from 10 to 90 min after H(2)O(2) treatment, levels were determined for respiratory complexes I, II, IV and V, and citrate synthase activities, mitochondrial Ca(2+) flux, intracellular oxidation, mitochondrial membrane potential and apoptotic progression. Complexes II and IV activity levels were significantly reduced within 20 min of H(2)O(2) exposure while complexes I and V, and citrate synthase were unaffected. Mitochondrial membrane potential declined after 20 and 60 min of H(2)O(2) exposure while intracellular oxidation, declining complex I activity and apoptotic progression were detectable only after 60 min. Measurement of mitochondrial Ca(2+) ([Ca(2+)](m)) using rhodamine 2 detected an early accumulation of [Ca(2+)](m) occurring between 5 and 10 min. Pretreatment of cardiomyocytes with either ruthenium red or cyclosporin A abrogated the H(...Continue Reading

Citations

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Jul 25, 2012·Ophthalmic Surgery, Lasers & Imaging : the Official Journal of the International Society for Imaging in the Eye·Matthew G FieldVictor M Elner
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Apr 14, 2006·The Journal of Pharmacology and Experimental Therapeutics·Ruijuan WangMasunori Matsuzaki
Apr 26, 2007·Molecular and Cellular Biochemistry·Xilin LongJosé Marín-García
Feb 1, 2007·Molecular and Cellular Biochemistry·YeQing PiJosé Marín-García
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