Acute toxic effect of sodium cyanide on cerebral cortex of rats and its mechanism

ObjectiveTo study the injury effect and its mechanism of sodium cyanide(NaCN) by acute exposure on cerebral cortex,especially on the mitochondria of cerebral cortex cells in rats.MethodAccording to study design,5、15、30、60 and 90min(after) injection i.p with sub-deadly dose(3.2mg/kg) of NaCN,the interrelated indices of oxidative-antioxidative system in cerebral cortex and the mitochondria of the cortex in rats were measured by colorimetric techniques.Meanwhile,the ultrastructural changes of cerebral cortex of the rats were examined by electron transmission microscopy.Additionally,the activities of the respiratory enzymes in mitochondria of cerebral cortex cells cultured with different concentrations of NaCN in vitro were also measured by Veitch and Dunkley's method.Result(1) In NaCN group,the activities of SOD,GPX,Na~(+)-K~(+)-ATPase,Ca~(2+)-Mg~(2+)-ATPase in the cortex and in the mitochondria were all decreased distinctly compared with the controls even 5min after injection of NaCN,while the activity of XOD showed definite increase in mitochondria seemed more significant(P0.001).(2) The damages in cortex of NaCN exposed rats showed more severe;edema, vacuolation and lysis could be seen clearly in neurons,neuroglial cells,especially their mitochondria by the electron transmission microscopy.(3) The activities of complex Ⅳ and II in respiratory chain of cortex exposed to NaCN in vitro was obviously decreased(P0.001),while the activity of complexⅠin the respiratory chain was increased dramatically(P0.001).ConclusionNaCN has the effect that may lead to dysequilibrium of oxidation/ antioxidation of cerebral cortex,especially the mitochondria,decline of the antioxidative ability,increase of the production of free radicals,decrease of activity of ATPase,and increase of electron-leaking in respiratory chain of mitochondria,which suggested that the injury in mitochondria of cerebral cortex might play an important role in cyanide-induced neurotoxicity.