Kosenko E A, Kaminskiĭ Iu G, Derkachev E F, Shchipakin V N, Kondrashova M N
Vopr Med Khim. 1982 Nov-Dec;28(6):87-90.
Administration of physiologically low doses of bicarbonate into rats caused an inhibition of oxidative phosphorylation and a transitory decrease in ATP content in liver mitochondria; at the same time, concentrations of malate and glutamate were unaltered and those of pyruvate and phosphoenolpyruvate were decreased. Insulin removed the bicarbonate effect on mitochondrial functions but affected only slightly the distribution of metabolites. Bicarbonate appears to activate pyruvate carboxylase and to inhibit succinate dehydrogenase as well as the operation of tricarboxylic acid cycle due to accumulation of oxaloacetate. The effect of insulin mimics acceleration of decarboxylation reactions in mitochondria.
给大鼠注射生理低剂量的碳酸氢盐会抑制氧化磷酸化,并使肝线粒体中的ATP含量暂时降低;与此同时,苹果酸和谷氨酸的浓度未改变,而丙酮酸和磷酸烯醇丙酮酸的浓度降低。胰岛素消除了碳酸氢盐对线粒体功能的影响,但对代谢物的分布影响甚微。由于草酰乙酸的积累,碳酸氢盐似乎激活了丙酮酸羧化酶并抑制了琥珀酸脱氢酶以及三羧酸循环的运行。胰岛素的作用类似于线粒体中脱羧反应的加速。