Acute hypoxia exacerbates inhibitory effects of sodium cyanide on energy metabolism in rat in vitro liver mitochondria
- VernacularTitle:急性低氧加重氰化钠对大鼠离体肝线粒体能量代谢的抑制作用
- Author:
Guoshou LU
;
Fuyu LIU
;
Yuqi GAO
;
Xiaohong YANG
;
Yongjun LUO
;
Wenxiang GAO
- Publication Type:Journal Article
- Keywords:
NaCN;
hypoxia;
mitochondrial oxidative consumption;
mitochondrial membrane potential;
the complex Ⅳ of mitochondria
- From:Journal of Third Military Medical University
2003;0(10):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate effect of sodium cyanide(NaCN)at different concentrations on the mitochondrial respiratory oxygen consumption,the mitochondrial membrane potential(MMP)and activity of the complex Ⅳ of mitochondrial breath train in in vitro liver mitochondria from the rats exposed to simulated high altitude hypoxia,and to explore the characteristics of energy metabolism in the mitochondria from the rats subjected to cyanide poisoning during acute hypoxia exposure.Methods Adult Sprague-Dawley(SD)rats were set randomly into control and acute hypoxia groups(n=8 in each group).The acute hypoxic rats were exposed to simulate 5 000 m high altitude in a hypobaric chamber 23 h/d for 3 d.Rats in the control group were bred in the normoxia condition at the same time.The liver mitochondria were isolated by centrifugation.Mitochondrial oxidative respiratory consumption and activity of the complex Ⅳ was measured by Clark electrode after the treatment of NaCN at 0,0.01,0.1 and 0.25 mmol/L respectively,so as to calculate mitochondrial state 3 respiration(ST3),state 4 respiration(ST4),respiratory control rate(RCR),the rate of oxidative phosphorylation(OPR),and oxygen consumption rate of the complex Ⅳ.MMP was detected by Rhodamine 123 method at the above-mentioned concentrations of NaCN.Results NaCNat0.01,0.1and0.25mmol/Linhibited the mito-chondrial oxidative respiratory function,and decreased MMP significantly.The inhibitory effects of NaCN onenergy metabolism in mitochondria was in a dose-dependent manner.Compared with the treatment of NaCN atthe corresponding concentration in the control group,mitochondrial function in the acute hypoxia group was in-hibited more seriously.Conclusion Acute hypoxia exacerbates the inhibitory effects of sodium cyanide on en-ergy metabolism in rat liver mitochondria.Its mechanism might be relevant to the decoupling of oxidative phos-phorylation,functional down-regulation of complexⅣin respiratory chain and changes of the mitochondrialmembrane potential in liver mitochondria from rats exposed to acute hypoxia.
