Antonucci 2019 Free Radic Biol Med

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Antonucci S, Mulvey JF, Burger N, Di Sante M, Hall AR, Hinchy EC, Caldwell ST, Gruszczyk AV, Deshwal S, Hartley RC, Kaludercic N, Murphy MP, Di Lisa F, Krieg T (2019) Selective mitochondrial superoxide generation in vivo is cardioprotective through hormesis. Free Radic Biol Med 134:678-687.

» PMID: 30731114 Open access

Antonucci S, Mulvey JF, Burger N, Di Sante M, Hall AR, Hinchy EC, Caldwell ST, Gruszczyk AV, Deshwal S, Hartley RC, Kaludercic N, Murphy MP, Di Lisa F, Krieg T (2019) Free Radic Biol Med

Abstract: Reactive oxygen species (ROS) have an equivocal role in myocardial ischaemia reperfusion injury. Within the cardiomyocyte, mitochondria are both a major source and target of ROS. We evaluate the effects of a selective, dose-dependent increase in mitochondrial ROS levels on cardiac physiology using the mitochondria-targeted redox cycler MitoParaquat (MitoPQ). Low levels of ROS decrease the susceptibility of neonatal rat ventricular myocytes (NRVMs) to anoxia/reoxygenation injury and also cause profound protection in an in vivo mouse model of ischaemia/reperfusion. However higher doses of MitoPQ resulted in a progressive alteration of intracellular [Ca2+] homeostasis and mitochondrial function in vitro, leading to dysfunction and death at high doses. Our data show that a primary increase in mitochondrial ROS can alter cellular function, and support a hormetic model in which low levels of ROS are cardioprotective while higher levels of ROS are cardiotoxic.

Keywords: Mitochondria, Reactive Oxygen Species, Ischaemia/Reperfusion injury Bioblast editor: Sobotka O


Labels: Pathology: Cardiovascular  Stress:Ischemia-reperfusion, Oxidative stress;RONS, Hypoxia  Organism: Rat