Institute of Theoretical and Experimental Biophysics RAS, Pushchino, Moscow Region, 142290, Russia.
J Bioenerg Biomembr. 2010 Dec;42(6):473-81. doi: 10.1007/s10863-010-9316-5. Epub 2010 Nov 17.
The mechanism of tissue protection from ischemic damage by activation of the mitochondrial ATP-dependent K(+) channel (mitoK(ATP)) remains unexplored. In this work, we have measured, using various approaches, the ATP-dependent mitochondrial K(+) transport in rats that differed in their resistance to hypoxia. The transport was found to be faster in the hypoxia-resistant rats as compared to that in the hypoxia-sensitive animals. Adaptation of animals to the intermittent normobaric hypoxia increased the rate of transport. At the same time, the intramitochondrial concentration of K(+) in the hypoxia-sensitive rats was higher than that in the resistant and adapted animals. This indicates that adaptation to hypoxia stimulates not only the influx of potassium into mitochondria, but also K(+)/H(+) exchange. When mitoK(ATP) was blocked, the rate of the mitochondrial H(2)O(2) production was found to be significantly higher in the hypoxia-resistant rats than that in the hypoxia-sensitive animals. The natural flavonoid-containing adaptogen Extralife, which has an evident antihypoxic effect, increased the rate of the mitochondrial ATP-dependent K(+) transport in vitro and increased the in vivo tolerance of hypoxia-sensitive rats to acute hypoxia 5-fold. The involvement of the mitochondrial K(+) transport in the mechanism of cell adaptation to hypoxia is discussed.
组织免受缺血性损伤的机制通过激活线粒体 ATP 依赖性钾通道（mitoK（ATP））仍然未知。在这项工作中，我们使用各种方法测量了对缺氧有不同抗性的大鼠的 ATP 依赖性线粒体钾转运。与缺氧敏感动物相比，发现缺氧抗性大鼠的转运速度更快。动物对间歇性常压低氧的适应增加了转运的速度。同时，缺氧敏感大鼠的线粒体内部钾浓度高于抗性和适应动物。这表明，对缺氧的适应不仅刺激了钾进入线粒体，还刺激了 K（+）/ H（+）交换。当 mitoK（ATP）被阻断时，在缺氧抗性大鼠中发现线粒体 H2O2 产生的速度明显高于缺氧敏感动物。天然含类黄酮的适应原 Extralife 具有明显的抗缺氧作用，它增加了体外线粒体 ATP 依赖性钾转运的速度，并使缺氧敏感大鼠对急性缺氧的体内耐受性增加了 5 倍。线粒体钾转运在细胞适应缺氧的机制中的参与正在讨论中。
