| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8326479 | The International Journal of Biochemistry & Cell Biology | 2007 | 12 Pages |
Abstract
We found that mPTP opening in reperfused hearts increased along with reperfusion time and concurs with cytochrome c release from mitochondria. Maximal cytochrome c release correlated with mitochondrial dysfunction and complete NAD+ deletion. Fully inserted BAX was detected early after reperfusion and remained unchanged during the evaluated reperfusion times. Remarkably, heart perfusion with Ru360, inhibited mPTP opening and BAX docking into the mitochondrial membranes, suggesting a mPTP upstream role on BAX migration/insertion.
Keywords
RU360Ac-DEVD-AFCANTVDACCCCPΔΨmMPTPI/R[Ca2+]mAIFmitochondrial permeability transitionmitochondrial permeability transition poreCSAischemia/reperfusionBaxadenine nucleotide translocatorTUNELApoptosiscytochrome ccyclosporin Aapoptosis-inducing factorterminal deoxynucleotidyl transferase-mediated dUTP nick-end labelingMitochondrial membrane potentialvoltage-dependent anion channelcarbonyl cyanide m-chlorophenyl hydrazone
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Authors
Francisco Correa, Virgilia Soto, Cecilia Zazueta,