绿豆线粒体呼吸链在不同电子传递途径中的电子漏

ELECTRON LEAKAGE THROUGH VARIOUS ELECTRON TRANSPORT PATHWAYS IN MUNG BEAN MITOCHONDRIA

绿豆线粒体的呼吸链在氧化不同底物时有不同的呼吸速率和电子漏速率，但是Ｏ^-_2／Ｏ_2比值较稳定。呼吸链部位Ⅱ的抑制剂抗霉素 Ａ对α－酮戊二酸、琥珀酸及苹果酸为底物时的电子漏速率和Ｏ^-_ｄ／Ｏ_2比值都有明显的促进作用，说明电子漏发生的位点可能在抗霉素Ａ的抑制点之前。呼吸链在氧化外源ＮＡＤＨ时，线粒体所产生的电子漏对氰化物、鱼藤酮、抗霉素Ａ及ＳＨＡＭ都不敏感，而对钙离子的螯合剂ＥＧＴＡ显著敏感，因此，依赖于钙离子的ＮＡＤＨ脱氢酶可能是线粒体产生电子漏的另一个位点。电子漏速率及Ｏ^-_2／Ｏ_2比值和线粒体的能量状态密切相关，在相同条件下状态４电子漏速率及Ｏ^-_2/O_2比值均高于状态 ３的。氰化物和ＳＨＡＭ对呼吸链的电子漏有抑制作用，说明电子漏可能与交替途径有关。

Electron leakage rate and respiratory rate were studied with mung beau mitochondria. Succinate, NADH, a-ketoglutarate, malate and NADH were strongly effective in supporting mitochondrial respiratory rate and electron leakage rate. The ratio of electron leakage rate and respiratory rate (O-2/O2) were not markedly different when different substrates were utilized in mung beau mitochondria. Electron leakage rate was promoted and respiratory rate was inhibited by antimycin-A when succinate, a-ketoglutarate and malate, not NADH, were oxidized. It seemed that the site of electron leakage in mitochondrial electron transport chain located before the site of antimycin-A block. When oxidized exogenous NADH, mitochondrial electron leakage was insensitive to CN-, rotenone, antimycin-A and SHAM, but EGTA, a Ca2+ chelator, was obviousely effective in inhibiting electron leakage. It suggested that Ca2+-dependent NADH dehydrogenase on the outside of mitochondrial inner membrane was one source of electron leakage in mung beau mitochondria. Electron leakage rate and O-2 /O2 are closely related with mitochondrial energic state. Mung beau mitochondria in state 4 presented a higher electron leakage rate and a higher O-2 /O2 as compared to those in state 3. Apart from exogenous NADH oxidation, both CN- and SHAM presented inhibitive effects on electron leakage, and these indicated that electron leakage was possibly related with alternative pathway.