NecroX-5 prevents hypoxia/reoxygenation injury by inhibiting the mitochondrial calcium uniporter

Abstract

Aims Preservation of mitochondrial function is essential to limit myocardial damage in ischaemic heart disease. We examined the protective effects and mechanism of a new compound, NecroX-5, on rat heart mitochondria in a hypoxia/reoxygenation (HR) model. Methods and Results NecroX-5 reduced mitochondrial oxidative stress, prevented the collapse in mitochondrial membrane potential, improved mitochondrial oxygen consumption, and suppressed mitochondrial Ca2+ overload during reoxygenation in an in vitro rat heart HR model. Furthermore, NecroX-5 reduced the ouabain-or histamine-induced increase in mitochondrial Ca2+. Conclusion These findings suggest that NecroX-5 may act as a mitochondrial Ca2+ uniporter inhibitor to protect cardiac mitochondria against HR damage. © 2011 The Author.