Marshansky V N, Novgorodov S A, Yaguzhinsky L S
FEBS Lett. 1983 Jul 11;158(1):27-30. doi: 10.1016/0014-5793(83)80669-3.
Lipid peroxidation in mitochondria induced by Fe2+ in the presence of ascorbate or by cumene hydroperoxide in the presence of phosphate results in a drop of the membrane potential and in K+ efflux. The inhibitors of ATP-synthetase (oligomycin and dicyclohexylcarbodiimide (DCCD)) are capable of preventing lipid peroxidation, stabilizing the membrane potential and inhibiting potassium efflux. The same effects are observed in the presence of ionol or alpha-tocopherol. In contrast to antioxidant protection the effects of oligomycin and DCCD are reversed by the uncoupler (FCCP). The functional link between non-enzymatic lipid peroxidation, proton conduction through Fo component of ATP-synthetase and induced cation transport is suggested.
在抗坏血酸存在的情况下,Fe2+ 诱导线粒体中的脂质过氧化,或者在磷酸盐存在的情况下,异丙苯过氧化氢诱导脂质过氧化,都会导致膜电位下降和钾离子外流。ATP 合成酶抑制剂(寡霉素和二环己基碳二亚胺(DCCD))能够防止脂质过氧化,稳定膜电位并抑制钾离子外流。在离子醇或α-生育酚存在的情况下也观察到相同的效果。与抗氧化保护作用相反,解偶联剂(FCCP)可逆转寡霉素和 DCCD 的作用。这表明非酶促脂质过氧化、质子通过 ATP 合成酶的 Fo 组分传导以及诱导的阳离子转运之间存在功能联系。