摘要
Mammalian mitochondria are sensitive targets of cytotoxic effect of superoxide and nitric oxide (NO).In this study we measured mitochondrial state 3, 4 respiration, respiratory control rate (RCR) and phosphor-oxygen ratio (P/O) to evaluate mitochondrial respiratory function (MRF) in cerebral ischemia and at 1, 3, 6, 24 and 48 h after reperfusion. We also observed the changes of MRF after giving N-nitro L- arginine (LNA) at various times. MRF was inhibited 30 min after cerebral ischemia. The major change was decrease in RCR, especially in the case of state 3 respiration. In the early stage of reperfusion, MRF recovered and state 3 was higher than the level of normal control. In later stage of reperfusion (at 6 h), obvious increase in state 4 led to decrease in RCR again. RCR was higher than that of reperfusion control by decreasing of state 4 when LNA was given at 1 h after reperfusion and 5 h thereafter; there were no change in MRF when LNA was given at the beginning of reperfusion. We concluded that MRF was further damaged, and ineffective oxygen consumption increased after reperfusion; LNA could protect MRF after reperfusion. Overproduction of endogenous NO has pathologic toxicity to mitochondria at 1- 2 h after reperfusion.
Mammalian mitochondria are sensitive targets of cytotoxic effect of superoxide and nitric oxide (NO).In this study we measured mitochondrial state 3, 4 respiration, respiratory control rate (RCR) and phosphor-oxygen ratio (P/O) to evaluate mitochondrial respiratory function (MRF) in cerebral ischemia and at 1, 3, 6, 24 and 48 h after reperfusion. We also observed the changes of MRF after giving N-nitro L- arginine (LNA) at various times. MRF was inhibited 30 min after cerebral ischemia. The major change was decrease in RCR, especially in the case of state 3 respiration. In the early stage of reperfusion, MRF recovered and state 3 was higher than the level of normal control. In later stage of reperfusion (at 6 h), obvious increase in state 4 led to decrease in RCR again. RCR was higher than that of reperfusion control by decreasing of state 4 when LNA was given at 1 h after reperfusion and 5 h thereafter; there were no change in MRF when LNA was given at the beginning of reperfusion. We concluded that MRF was further damaged, and ineffective oxygen consumption increased after reperfusion; LNA could protect MRF after reperfusion. Overproduction of endogenous NO has pathologic toxicity to mitochondria at 1- 2 h after reperfusion.
