Rehncrona S, Hauge H N, Siesjö B K
Laboratory of Experimental Brain Research, University of Lund, Sweden.
J Cereb Blood Flow Metab. 1989 Feb;9(1):65-70. doi: 10.1038/jcbfm.1989.9.
The influence of lactic acidosis and of extreme hypercapnia on free radical generation and lipid peroxidation in brain tissues was studied. Cortical homogenates were prepared from the rat brain in a bicarbonate buffer and incubated for 60 min. Lipid peroxidation was evaluated by measurements of thiobarbituric acid reactive (TBAR) material and alpha-tocopherol analysis. The pH during incubations were decreased to 6.10-6.20 by either lactic acid administration or equilibration with 60% CO2 gas in paired experiments. In homogenates treated with lactic acid there was a 20-fold increase in TBAR material and the alpha-tocopherol concentration decreased to approximately 60% of control. There was only a 10-fold increase in TBAR material and no change in alpha-tocopherol concentration if acidosis was induced by CO2. These differences between lactic acidosis and hypercapnic acidosis were statistically highly significant. The results indicate that lactic acidosis has a more pronounced effect in augmenting free radical generation in brain tissues than acidosis due to an increase in CO2 tension. It is suggested that this effect of lactic acid is mediated by increased dissociation of catalytic iron from proteins of the transferrin type.
研究了乳酸酸中毒和极度高碳酸血症对脑组织中自由基生成和脂质过氧化的影响。在碳酸氢盐缓冲液中从大鼠脑制备皮质匀浆，并孵育60分钟。通过测量硫代巴比妥酸反应性（TBAR）物质和α-生育酚分析来评估脂质过氧化。在配对实验中，通过给予乳酸或用60%二氧化碳气体平衡，使孵育期间的pH降至6.10 - 6.20。在用乳酸处理的匀浆中，TBAR物质增加了20倍，α-生育酚浓度降至对照的约60%。如果由二氧化碳诱导酸中毒，TBAR物质仅增加10倍，α-生育酚浓度无变化。乳酸酸中毒和高碳酸血症性酸中毒之间的这些差异在统计学上具有高度显著性。结果表明，与因二氧化碳张力增加导致的酸中毒相比，乳酸酸中毒在增强脑组织自由基生成方面具有更显著的作用。提示乳酸的这种作用是由转铁蛋白类型蛋白质中催化铁的解离增加介导的。
