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.
ABSTRACT
Objective To investigate the effects of hypoxia and sodium cyanide(NaCN)on oxidative stress in rabbit arterial blood.Methods An artificial hypobaric hypoxia chamber was used to simulate 4 000-meter high altitude.Twenty rabbits were randomly divided into 4 groups:hypoxia group with high-or low-dose,non-hypoxia with high-or low-dose.The animals in the non-hypoxia groups were operated under normal circumstances while those in hypoxia groups were subjected to chamber in low pressure for 72 h before receiving the hypoxia experiments.Femoral arterial cannulation was performed on all animals under anesthetization with pentobarbital sodium(30 mg/kg,iv)and NaCN(ip)at the doses of 1.5 mg/kg and 2 mg/kg.Blood samples were collected at 10 min before intoxication,and 5,10,15,20,30,60,120 and 180 min after intoxication and blood seperation was conducted.The activity of superoxide dismutase(SOD),contents of reduced glutathione(GSH)and malondialdehyde(MDA)were determined.Results The MDA content was significantly increased(P