Takayanagi R, Takeshige K, Minakami S
Biochem J. 1980 Dec 15;192(3):853-60. doi: 10.1042/bj1920853.
Malondialdehyde formations by bovine heart submitochondrial particles supported by NADH or NADPH in the presence of ADP and FeCl3 was studied. The NADH-dependent reaction was maximal at very low rate of electron input from NADH to the respiratory chain and it decreased when the rate became high. The reaction was stimulated by rotenone and inhibited by antimycin A when the input was fast, whereas it was not affected by the inhibitors when the input was slow. The input rate of the electrons from NADPH was also so low that the reaction supported by NADPH was not affected by the inhibitors. Most of the endogenous ubiquinone in the particles treated with antimycin A was reduced by NADH even in the presence of ADP-Fe3+ chelate, but uniquinone was not reduced by NADPH when ADP-Fe3+ was present. Succinate strongly inhibited both NADH- and NADPH-dependent lipid peroxidation. The inhibition was abolished when uniquinone was removed from the particles, and it appeared again when uniquinone was reincorporated into the particles. Reduced uniquinone-2 also inhibited the peroxidation, but duroquinol, which reduces cytochrome b without reducing endogenous uniquinone, did not. Thus the malondialdehyde formation appeared to be inversely related to the extent of the reduction of endogenous uniquinone. These observations suggest that both NADH- and NADPH-dependent liquid-peroxidation reactions are closely related to the respiratory chain and that the peroxidation is controlled by the concentration of reduced ubiquinone.
研究了在ADP和FeCl3存在的情况下，由NADH或NADPH支持的牛心亚线粒体颗粒形成丙二醛的情况。依赖NADH的反应在从NADH到呼吸链的电子输入速率非常低时达到最大值，当速率升高时反应会下降。当电子输入快速时，鱼藤酮会刺激该反应，抗霉素A会抑制该反应，而当输入缓慢时，抑制剂对其没有影响。来自NADPH的电子输入速率也很低，以至于由NADPH支持的反应不受抑制剂影响。即使在存在ADP-Fe3+螯合物的情况下，用抗霉素A处理的颗粒中的大多数内源性泛醌也会被NADH还原，但当存在ADP-Fe3+时，泛醌不会被NADPH还原。琥珀酸强烈抑制依赖NADH和NADPH的脂质过氧化。当从颗粒中去除泛醌时，这种抑制作用消失，当泛醌重新掺入颗粒中时，抑制作用又会出现。还原型泛醌-2也会抑制过氧化作用，但二氢醌（它能还原细胞色素b而不还原内源性泛醌）则不会。因此，丙二醛的形成似乎与内源性泛醌的还原程度呈负相关。这些观察结果表明，依赖NADH和NADPH的脂质过氧化反应都与呼吸链密切相关，并且过氧化作用受还原型泛醌浓度的控制。
