Intermittent hypoxia exposure prevents mtDNA deletion and mitochondrial structure damage produced by ischemia/reperfusion injury.
In the present study, polymerase chain reaction (PCR) was conducted to determine mtDNA(4834) deletion, and myocardial ultrastructure was visualized by electron microscope to see whether intermittent hypoxia (high altitude) adaptation exerts some action on mitochondria against ischemia/reperfusion injury. Myocardial ischemia/reperfusion in isolated perfused rat hearts induced severe damage to the ultrastructure of myocardial mitochondria and mtDNA4834 deletion down to 87.5% of normoxia rats. After the rats were exposed to intermittent hypoxia (5000 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.
Zhong
N
N
Physiological Laboratory of Hypoxia, Shanghai Institute of Physiology, Chinese Academy of Sciences, Shanghai 200031, China. znzhou@server.shcnc.ac.cn
Zhang
Y
Y
Zhu
H F
HF
Zhou
Z N
ZN
D000818:Animals; D001483:Base Sequence; D004249:DNA Damage; D004272:DNA, Mitochondrial / Q000235:genetics*; D000860:Hypoxia; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D008969:Molecular Sequence Data; D015428:Myocardial Reperfusion Injury / Q000473:pathology*; D009206:Myocardium / Q000648:ultrastructure*; D016133:Polymerase Chain Reaction; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley
D004272:DNA, Mitochondrial