Intermittent hypoxia exposure prevents mtDNA deletion and mitochondrial structure damage produced by ischemia/reperfusion injury
10.3321/j.issn:0371-0874.2000.05.005
- VernacularTitle:间歇性低氧防止缺血再灌注损伤引起的线粒体结构损伤和mtDNA片段缺失
- Author:
Ning ZHONG
1
;
Yi ZHANG
;
Hai-Feng ZHU
;
Zhao-Nian ZHOU
Author Information
1. 中国科学院上海生理学研究所
- Keywords:
mitochondrial DNA;
polymerase chain reaction;
ischemia/reperfusion injury;
intermittent hypoxia;
ultrastructure
- From:
Acta Physiologica Sinica
2000;52(5):375-380
- CountryChina
- Language:Chinese
-
Abstract:
In the present study, polymerase chain reaction (PCR) was conducted to determine mtDNA4834 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 mtDNA4834 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.
