一氧化碳中毒对大鼠脑的生化影响，特别涉及血液碳氧血红蛋白和脑线粒体细胞色素氧化酶活性

Biochemical effects of carbon monoxide poisoning in rat brain with special reference to blood carboxyhemoglobin and cerebral cytochrome oxidase activity.

作者信息

Savolainen H, Kurppa K, Tenhunen R, Kivistö H

出版信息

Neurosci Lett. 1980 Oct 2;19(3):319-23. doi: 10.1016/0304-3940(80)90281-5.

Abstract

Male Wistar rats exposed to 1000 ppm carbon monoxide for 3 h showed a rapid removal of carbon monoxide from the blood, and a cerebral cytochrome oxidase activity within the control range immediately after the end of the exposure. The cytochrome oxidase activity decreased while carboxyhemoglobin concentration diminished during the reoxygenation period. The effect might have been caused through a loss of mitochondria by increased lipid peroxidation as cerebral glutathione concentration decreased and lysosomal acid proteinase activity increased in glial cell fractions. The present results seem to indicate that the cerebral cytochrome oxidase may not be specifically inhibited in non-lethal carbon monoxide poisoning despite its proven interactions in vitro.

摘要

将雄性Wistar大鼠暴露于1000 ppm一氧化碳中3小时，结果显示血液中的一氧化碳迅速清除，且在暴露结束后即刻，大脑细胞色素氧化酶活性处于对照范围内。在复氧期，随着碳氧血红蛋白浓度降低，细胞色素氧化酶活性也下降。这种效应可能是由于脂质过氧化增加导致线粒体丢失所致，因为神经胶质细胞组分中的脑谷胱甘肽浓度降低，溶酶体酸性蛋白酶活性增加。目前的结果似乎表明，尽管在体外已证实存在相互作用，但在非致死性一氧化碳中毒中，大脑细胞色素氧化酶可能不会受到特异性抑制。