Glinn M, Ernster L, Lee C P
Department of Biochemistry, Wayne State University School of Medicine, Detroit, Michigan 48201.
Arch Biochem Biophys. 1991 Oct;290(1):57-65. doi: 10.1016/0003-9861(91)90591-6.
Initiation of lipid peroxidation in the inner mitochondrial membrane was investigated using respiratory substrates and inhibitors and various iron chelates. An iron chelate was required for initiation of lipid peroxidation in the presence of either NADH or NADPH. The two nicotinamide nucleotides exhibited different activities in initiating lipid peroxidation with regard to concentration and to the effects of rotenone and rhein. Succinate and both nicotinamide nucleotides supported lipid peroxidation in the presence of thenoyl trifluoroacetone (TTFA), without a requirement for exogenously added iron. ADP stimulated lipid peroxidation in the case of NAD(P)H and TTFA, but inhibited it in the case of succinate and TTFA. Lipid peroxidation is thought to be enzymatically induced in both the NADH and the succinate dehydrogenase regions of the respiratory chain, and evidence is presented for a novel pathway of NADPH oxidation that may also be involved. Possible initiation mechanisms are discussed.
利用呼吸底物、抑制剂以及各种铁螯合物，对内线粒体膜中脂质过氧化的引发过程进行了研究。在存在烟酰胺腺嘌呤二核苷酸（NADH）或烟酰胺腺嘌呤二核苷酸磷酸（NADPH）的情况下，引发脂质过氧化需要一种铁螯合物。就浓度以及鱼藤酮和大黄酸的影响而言，这两种烟酰胺核苷酸在引发脂质过氧化方面表现出不同的活性。在存在噻吩甲酰三氟丙酮（TTFA）的情况下，琥珀酸以及两种烟酰胺核苷酸都能支持脂质过氧化，且无需外源添加铁。在NAD（P）H和TTFA的情况下，二磷酸腺苷（ADP）会刺激脂质过氧化，但在琥珀酸和TTFA的情况下则会抑制脂质过氧化。脂质过氧化被认为在呼吸链的NADH和琥珀酸脱氢酶区域都是由酶诱导的，并且有证据表明可能还涉及一种新的NADPH氧化途径。文中讨论了可能的引发机制。
