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Biomedical Engineering and Bioengineering Commons™
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Full-Text Articles in Biomedical Engineering and Bioengineering
Tyrosine Nitration Of Voltage-Dependent Anion Channels In Cardiac Ischemia-Reperfusion: Reduction By Peroxynitrite Scavenging, Meiying Yang, Amadou K.S. Camara, Bassam T. Wakim, Yifan Zhou, Ashish K. Gadicherla, Wai-Meng Kwok, David F. Stowe
Tyrosine Nitration Of Voltage-Dependent Anion Channels In Cardiac Ischemia-Reperfusion: Reduction By Peroxynitrite Scavenging, Meiying Yang, Amadou K.S. Camara, Bassam T. Wakim, Yifan Zhou, Ashish K. Gadicherla, Wai-Meng Kwok, David F. Stowe
Biomedical Engineering Faculty Research and Publications
Excess superoxide (O2−) and nitric oxide (NO) forms peroxynitrite (ONOO−) during cardiac ischemia reperfusion (IR) injury, which in turn induces protein tyrosine nitration (tyr-N). Mitochondria are both a source of and target for ONOO−. Our aim was to identify specific mitochondrial proteins that display enhanced tyr-N after cardiac IR injury, and to explore whether inhibiting O2−/ONOO− during IR decreases mitochondrial protein tyr-N and consequently improves cardiac function. We show here that IR increased tyr-N of 35 and 15 kDa mitochondrial proteins using Western blot analysis with 3-nitrotyrosine antibody. Immunoprecipitation …
Damage To Mitochondrial Complex I During Cardiac Ischemia Reperfusion Injury Is Reduced Indirectly By Anti-Anginal Drug Ranolazine, Ashish K. Gadicherla, David F. Stowe, William E. Antholine, Meiying Yang, Amadou K.S. Camara
Damage To Mitochondrial Complex I During Cardiac Ischemia Reperfusion Injury Is Reduced Indirectly By Anti-Anginal Drug Ranolazine, Ashish K. Gadicherla, David F. Stowe, William E. Antholine, Meiying Yang, Amadou K.S. Camara
Biomedical Engineering Faculty Research and Publications
Ranolazine, an anti-anginal drug, is a late Na+ channel current blocker that is also believed to attenuate fatty acid oxidation and mitochondrial respiratory complex I activity, especially during ischemia. In this study, we investigated if ranolazine's protective effect against cardiac ischemia/reperfusion (IR) injury is mediated at the mitochondrial level and specifically if respiratory complex I (NADH Ubiquinone oxidoreductase) function is protected. We treated isolated and perfused guinea pig hearts with ranolazine just before 30 min ischemia and then isolated cardiac mitochondria at the end of 30 min ischemia and/or 30 min ischemia followed by 10 min reperfusion. We utilized …
Enhanced Charge-Independent Mitochondrial Free Ca2+ And Attenuated Adp-Induced Nadh Oxidation By Isoflurane: Implications For Cardioprotection, Bhawana Agarwal, Amadou K.S. Camara, David F. Stowe, Zeljko J. Bosnjak, Ranjan K. Dash
Enhanced Charge-Independent Mitochondrial Free Ca2+ And Attenuated Adp-Induced Nadh Oxidation By Isoflurane: Implications For Cardioprotection, Bhawana Agarwal, Amadou K.S. Camara, David F. Stowe, Zeljko J. Bosnjak, Ranjan K. Dash
Biomedical Engineering Faculty Research and Publications
Modulation of mitochondrial free Ca2 + ([Ca2 +]m) is implicated as one of the possible upstream factors that initiates anesthetic-mediated cardioprotection against ischemia–reperfusion (IR) injury. To unravel possible mechanisms by which volatile anesthetics modulate [Ca2 +]m and mitochondrial bioenergetics, with implications for cardioprotection, experiments were conducted to spectrofluorometrically measure concentration-dependent effects of isoflurane (0.5, 1, 1.5, 2 mM) on the magnitudes and time-courses of [Ca2 +]m and mitochondrial redox state (NADH), membrane potential (ΔΨm), respiration, and matrix volume. Isolated mitochondria from rat hearts were energized with 10 …