Ferranti Renato, da Silva Mirian M, Kowaltowski Alicia J
Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, SP, 05508-900, Brazil.
FEBS Lett. 2003 Feb 11;536(1-3):51-5. doi: 10.1016/s0014-5793(03)00007-3.
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 H(2)O(2) release is observed when mitoK(ATP) is active both with respiration stimulated by oxidative phosphorylation and when ATP synthesis is inhibited. In addition, decreased H(2)O(2) release is observed when mitochondrial Delta pH 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.
线粒体ATP敏感性钾通道（mitoK(ATP)）开放先前已被证明可通过刺激钾离子跨内膜循环，略微增加呼吸作用并降低膜电位。在此我们表明，mitoK(ATP)开放可减少心脏、肝脏和脑线粒体中活性氧的生成。当mitoK(ATP)激活时，无论是在氧化磷酸化刺激呼吸作用的情况下，还是在ATP合成受到抑制时，均观察到过氧化氢释放减少。此外，当线粒体ΔpH升高时，也观察到过氧化氢释放减少，这是mitoK(ATP)开放时预期会出现的效应。我们得出结论，mitoK(ATP)是触发轻度解偶联、防止活性氧释放的有效途径。
