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   NaCN at 0.01

0.1 and 0.25 mmol/L inhibited the mitochondrial oxidative respiratory function

and decreased MMP significantly. The inhibitory effects of NaCN on energy metabolism in mitochondria was in a dose-dependent manner. Compared with the treatment of NaCN at the corresponding concentration in the control group

mitochondrial function in the acute hypoxia group was inhibited more seriously.    Conclusion   Acute hypoxia exacerbates the inhibitory effects of sodium cyanide on energy metabolism in rat liver mitochondria. Its mechanism might be relevant to the decoupling of oxidative phosphorylation

functional down-regulation of complex  Ⅳ in respiratory chain and changes of the mitochondrial membrane potential in liver mitochondria from rats exposed to acute hypoxia.