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Intermittent hypoxia exposure prevents mtDNA deletion and mitochondrial structure damage produced by ischemia/reperfusion injury

Zhong Ning, Zhang Yi, Zhu Haifeng, Zhou Zhaonian

Physiological Laboratory of Hypoxia,Shanghai Institute of Physiology,Chinese Academy of Sciences.Shanghai 200031

Abstract

Myocardial ischemia/reperfusion in isolated perfused rat hearts induced severe damage to the ultrastructure of myocardial mitochondria and mtDNA~(4834) deletion down to 87.5% of normoxia rats. After the rats were exposed to intermittent hypoxia (5 000 m; 6 h/d for 28 d), the myocardial structure was well reserved and mtDNA~(4834) deletion dropped to 28.57% of control (P<0.05). It is suggested that intermittent hypoxia adaptation prevents mtDNA deletion, and preserves normal structure of mitochondria, which would be beneficial to the maintenance of normal mitochondrial function, and increases tolerance of myocardium against ischemia/reperfusion injury.

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Citing This Article：

Zhong Ning, Zhang Yi, Zhu Haifeng, Zhou Zhaonian. Intermittent hypoxia exposure prevents mtDNA deletion and mitochondrial structure damage produced by ischemia/reperfusion injury. Acta Physiol Sin 2000; 52 (5): 375-380 (in Chinese with English abstract).