Mitochondrial ATP‐sensitive K+ channel opening decreases reactive oxygen species generation

FEBS Letters

Kowaltowski, Alicia J¹  da Silva, Mirian M¹  Ferranti, Renato¹ 

[1] Departamento de Bioquı́mica, Instituto de Quı́mica, Universidade de São Paulo, São Paulo, SP, 05508-900, Brazil

关键词: Free radicals;    Ischemia;    Preconditioning;    Oxidative stress;    Diazoxide;    BSA;    bovine serum albumin;    DCFDA;    dichlorofluorescein diacetate;    DZX;    diazoxide;    FCCP;    carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone;    H2DCFDA;    dichlorodihydrofluorescein diacetate;    HRP;    horseradish peroxidase;    mitoKATP;    mitochondrial ATP-sensitive K+ channel;    Pi;    inorganic phosphate;    ROS;    reactive oxygen species;    S.E.M.;    standard error;    ΔΨ;    mitochondrial membrane potential;   

DOI  :  10.1016/S0014-5793(03)00007-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Mitochondrial ATP-sensitive K⁺ channel (mitoK_ATP) opening was shown previously to slightly increase respiration and decrease the membrane potential by stimulating K⁺ cycling across the inner membrane. Here we show that mitoK_ATP opening reduces reactive oxygen species generation in heart, liver and brain mitochondria. Decreased H₂O₂ release is observed when mitoK_ATP is active both with respiration stimulated by oxidative phosphorylation and when ATP synthesis is inhibited. In addition, decreased H₂O₂ release is observed when mitochondrial ΔpH is enhanced, an effect expected to occur when mitoK_ATP is open. We conclude that mitoK_ATP is an effective pathway to trigger mild uncoupling, preventing reactive oxygen species release.

【 授权许可】

Unknown