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目的：研究细菌内毒素（LPS）、磷脂酶A2（PLA2）及自由基对质子跨膜转运及H+－ATP酶的影响。方法：采用正常大鼠，制备线粒体、亚线粒体（SMP），用SMP与LPS（100μg／ml）、PLA2（10u／ml）、FeSO4；／VitC（30／900μmol／L）分别共同温育（30C，30min），用ACMA荧光淬灭法测定质子跨膜转运能力。线粒体与不同浓度LPS、PLA2和FeSO4／VitC共同孵育，测定H+－ATP酶、PLA2、MDA。结果：LPS、PLA2、FeSO4／VitC可致亚线粒体ACMA荧光淬灭显著改变，LPS可引起线粒体膜PLA2活性、MDA含量升高（P＜0．05），LPS、PLA2可引起H+－ATP酶的活性进行性下降，小剂量FeSO4／VitC引起H+－ATP酶活性升高，大剂量FeSO4／VitC引起H+－ATP酶活性降低。结论：LPS、PLA2、LPO是造成质子转运能力下降的重要原因．自由基与H+－ATP酶损伤密切相关。
Objective: To study the effects of bacterial endotoxin (LPS), phospholipase A2 (PLA2) and free radicals on proton transmembrane transport and H + -ATPase. Methods: Mitochondrial and mitochondrial mitochondria (SMP) were prepared from normal rats and incubated with SMP and LPS (100μg / ml), PLA2 (10u / ml), and FeSO4 and / VitC (30/900μmol / , 30 min). The proton transmembrane transport ability was determined by ACMA fluorescence quenching method. Mitochondria were incubated with different concentrations of LPS, PLA2 and FeSO4 / VitC to determine H + -ATPase, PLA2 and MDA. Results: LPS, PLA2 and FeSO4 / VitC could significantly change the fluorescence intensity of mitochondrial ACMA, LPS could induce PLA2 activity and MDA content in mitochondrial membrane (P <0.05). LPS and PLA2 could induce H + -ATPase Activity decline, small doses of FeSO4 / VitC caused by H + -ATPase activity increased, high-dose FeSO4 / VitC caused H + -ATPase activity decreased. Conclusion: LPS, PLA2 and LPO are the important reasons for the decrease of proton transport capacity. Free radicals and H + -ATP enzyme damage are closely related.