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Biphasic effect of nitric oxide on the cardiac voltage‐dependent anion channel
Author(s) -
Cheng Qunli,
Sedlic Filip,
Pravdic Danijel,
Bosnjak Zeljko J.,
Kwok Wai-Meng
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.12.008
Subject(s) - voltage dependent anion channel , nitric oxide , chemistry , biophysics , mitochondrial permeability transition pore , mitochondrion , scavenger , inner mitochondrial membrane , ion , biochemistry , apoptosis , bacterial outer membrane , radical , biology , organic chemistry , escherichia coli , programmed cell death , gene
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.