The effects of toxic substance D1,extracted from burn eschars,on the hepatic mitochondrial respiratory function and its damages to the respirtatory chain were observed in the rat.It was found that the rate of stste 3r...The effects of toxic substance D1,extracted from burn eschars,on the hepatic mitochondrial respiratory function and its damages to the respirtatory chain were observed in the rat.It was found that the rate of stste 3respiration was inhibited and that of state 4 respiration stimulated by D1.There was an obvious dosage-effect relationship between D1 dosage and the rate of oxygen consumption, that is,the changes of the rate was slow in the range of low dosage and fast in the range of high dosage. The point of change was at 1 mg/ml of D1 concentration.The ratio of FCCP-stimulated respiration rate/state 4 respiration rate was decreased when D1 dosage was increased.The results of experiments were similar whether glutamate+malate or succinate were used as the substrate. The point of change was also at 1 mg/ml of D1 concentration. The decrease of FCCP-stimulated rate/state 4rate implied that the respiratory chain was damaged.But complex Ⅳ-the terminal segment of the chain-remained intact. Thus, the site of damage must be somewhere in complexesⅠ￣Ⅲ and/or complexes Ⅱ￣Ⅲ. Since NADH dehydrogenase and succinate dehydrogenase-the main enzymes in complexesⅠand Ⅱ-were not affected by D1 but NADH: cytochrome c reductase and succinate:cytochrome c reductase markedly inhibited, the site of damage was most likely located in complex Ⅲ-the bc1 complex.展开更多
文摘The effects of toxic substance D1,extracted from burn eschars,on the hepatic mitochondrial respiratory function and its damages to the respirtatory chain were observed in the rat.It was found that the rate of stste 3respiration was inhibited and that of state 4 respiration stimulated by D1.There was an obvious dosage-effect relationship between D1 dosage and the rate of oxygen consumption, that is,the changes of the rate was slow in the range of low dosage and fast in the range of high dosage. The point of change was at 1 mg/ml of D1 concentration.The ratio of FCCP-stimulated respiration rate/state 4 respiration rate was decreased when D1 dosage was increased.The results of experiments were similar whether glutamate+malate or succinate were used as the substrate. The point of change was also at 1 mg/ml of D1 concentration. The decrease of FCCP-stimulated rate/state 4rate implied that the respiratory chain was damaged.But complex Ⅳ-the terminal segment of the chain-remained intact. Thus, the site of damage must be somewhere in complexesⅠ￣Ⅲ and/or complexes Ⅱ￣Ⅲ. Since NADH dehydrogenase and succinate dehydrogenase-the main enzymes in complexesⅠand Ⅱ-were not affected by D1 but NADH: cytochrome c reductase and succinate:cytochrome c reductase markedly inhibited, the site of damage was most likely located in complex Ⅲ-the bc1 complex.
