Cherkasskaia M D, Iasaĭtis A A
Vopr Med Khim. 1976 Jul-Aug;22(4):443-8.
Acetylsalicylate (2-5 mM) inhibited phosphorylating (condition III) and uncoupled respiration of rat liver mitochondria in vitro, when succinate and glutamate were used as substrates of oxidation. Lower concentrations of acetylsalicylate did not cause the uncoupling effect. Antirheumatic drug 2,3-dihydroxybenzoate activated the phosphorylation in mitochondria, if it was added up to concentrations of 0.5-5.0 mM for succinate and 0.5 mM for glutamate. An increase of 2,3-dihydroxybenzoate concentration was accompanied by gradual inhibition of phosphorylating and uncoupled oxidation of succinate; activation of the respiration was completely abolished by addition of ADP, DNP and 2,3-dihydroxybenzoate (20 mM). The data obtained suggest that the uncoupling effect of salicylate, which is formed by hydrolysis of acetylsalicylate in the organism, might be responsible for the toxic effect of the latter.
当使用琥珀酸和谷氨酸作为氧化底物时，乙酰水杨酸（2 - 5 mM）在体外抑制大鼠肝线粒体的磷酸化作用（条件III）并使呼吸解偶联。较低浓度的乙酰水杨酸不会引起解偶联效应。抗风湿药物2,3 - 二羟基苯甲酸可激活线粒体中的磷酸化作用，如果将其添加至琥珀酸浓度为0.5 - 5.0 mM、谷氨酸浓度为0.5 mM时。随着2,3 - 二羟基苯甲酸浓度的增加，琥珀酸的磷酸化作用逐渐受到抑制且其氧化解偶联；添加ADP、二硝基苯酚（DNP）和2,3 - 二羟基苯甲酸（20 mM）后，呼吸激活作用完全消失。所获得的数据表明，机体中乙酰水杨酸水解形成的水杨酸的解偶联效应可能是后者产生毒性作用的原因。
