Inhibition of cytochrome c release by 10-N-nonyl acridine orange, a cardiolipin-specific dye, during myocardial ischemia-reperfusion in the rat

American Journal of Physiology. Heart and Circulatory Physiology
Guo-Xing ZhangMiyako Takaki

Abstract

The release of cytochrome c from the mitochondria to the cytosol is a critical step for downstream caspase-mediated apoptotic signal transduction in ischemia-reperfusion (I/R)-induced myocardial tissue injury. 10-N-nonyl acridine orange (NAO), a cardiolipin-specific dye, has been shown to inhibit Bid-mediated cytochrome c release from isolated mitochondria in vitro; however, the possible protective effects of NAO and the mechanisms underlying the protection from myocardial I/R-induced tissue injury in a rat model are unknown. Male Sprague-Dawley rats were subjected to a 30-min coronary arterial occlusion followed by reperfusion. All rats received either vehicle or NAO (100 microg/kg iv) 10 min before the occlusion. The infarct size in the heart at 24 h after reperfusion was significantly reduced in NAO-treated rats compared with vehicle-treated rats. NAO treatment significantly reduced the cytosolic cytochrome c contents and caspase-9 activity in the ischemic region but did not affect caspase-8 activity. Furthermore, NAO treatment markedly suppressed the translocation of truncated Bid, a proapoptotic Bcl-2 family member, to the mitochondrial fraction. NAO also suppressed the mitochondrial swelling and oxygen uptake stimulated b...Continue Reading

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Citations

Nov 6, 2013·Chemistry and Physics of Lipids·Quan He, Xianlin Han
Jul 16, 2011·Journal of Molecular and Cellular Cardiology·Giovanni FajardoDaniel Bernstein
Jul 6, 2010·Mitochondrion·Lucia BiasuttoJiri Neuzil
Nov 6, 2010·Micron : the International Research and Review Journal for Microscopy·Gi-Ja LeeHun-Kuk Park
Sep 16, 2019·Biochimica Et Biophysica Acta. Biomembranes·Angelique CamilleriNeville Vassallo
Jul 30, 2019·ACS Chemical Neuroscience·Stephanie GhioNeville Vassallo

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