Journal
JOURNAL OF BIOENERGETICS AND BIOMEMBRANES
Volume 42, Issue 6, Pages 473-481Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10863-010-9316-5
Keywords
Mitochondrial ATP-dependent K+ channel; K+/H+ exchange; ROS; Hypoxia; Adaptation; Flavonoid-containing adaptogen
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Funding
- Russian Foundation for Basic Research [10-04-00920a]
- International Science & Technology Center [3301]
- Russian Ministry for Education [3840]
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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 H2O2 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.
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