Takeshige K, Minadami S
J Biochem. 1975 May;77(5):1067-73. doi: 10.1093/oxfordjournals.jbchem.a130807.
Electron transport particles (ETP) prepared from beef heart mitochondria formed malondialdehyde by NADPH-dependent lipid peroixidation in the presence of ferric ions and ADP or ATP. The reaction was inhibited by MnCl2, EDTA, or radical scavengers, but was not inhibited by p-hydroxymercuribenzoate (PHMB) or respiratory chain inhibitors. The oxidation of NADPH and oxygen consumption by ETP were activated by the addition of ferric ions and APT, and inhibited by inhibitors of lipid peroxidation. This peroxidation system was apparently different from those of liver microsomes and mitochondria as regards the effect of PHMB, optimal pH and the concentration of NADPH for half-maximal reaction velocity.
从牛心线粒体制备的电子传递颗粒（ETP）在铁离子以及ADP或ATP存在的情况下，通过NADPH依赖的脂质过氧化作用形成丙二醛。该反应受到氯化锰、乙二胺四乙酸（EDTA）或自由基清除剂的抑制，但不受对羟基汞苯甲酸（PHMB）或呼吸链抑制剂的抑制。ETP对NADPH的氧化作用以及氧气消耗通过添加铁离子和三磷酸腺苷（ATP）而被激活，并受到脂质过氧化作用抑制剂的抑制。就PHMB的作用、最适pH值以及达到最大反应速度一半时的NADPH浓度而言，该过氧化系统明显不同于肝微粒体和线粒体的过氧化系统。
