| Literature DB >> 21156174 |
Qunli Cheng1, Filip Sedlic, Danijel Pravdic, Zeljko J Bosnjak, Wai-Meng Kwok.
Abstract
Nitric oxide (NO·) effects on the cardiac mitochondrial voltage-dependent anion channel (VDAC) are unknown. The effects of exogenous NO· on VDAC purified from rat hearts were investigated in this study. When incorporated into lipid bilayers, VDAC was inhibited directly by an NO· donor, PAPA NONOate, in a concentration-dependent biphasic manner. This was prevented by an NO· scavenger, 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide. The effect paralleled that of NO() in delaying the opening of the mitochondrial permeability transition (PT) pore. These biphasic effects on the cardiac VDAC and the mitochondrial PT pore reveal a tandem impact of NO() on the two mitochondrial entities.Entities:
Mesh:
Substances:
Year: 2010 PMID: 21156174 PMCID: PMC3035949 DOI: 10.1016/j.febslet.2010.12.008
Source DB: PubMed Journal: FEBS Lett ISSN: 0014-5793 Impact factor: 4.124