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首页> 外文期刊>Biochemistry >Ca2+-induced increased lipid packing and domain formation in submitochondrial particles. A possible early step in the mechanism of Ca2+-stimulated generation of reactive oxygen species by the respiratory chain.
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Ca2+-induced increased lipid packing and domain formation in submitochondrial particles. A possible early step in the mechanism of Ca2+-stimulated generation of reactive oxygen species by the respiratory chain.

机译：Ca2 +诱导的线粒体颗粒中脂质堆积和结构域形成增加。 Ca 2+刺激呼吸链产生活性氧的机理中可能的早期步骤。

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摘要

Ca2+ and P(i) accumulation by mitochondria triggers a number of alterations leading to nonspecific increase in inner membrane permeability [Kowaltowski, A. J., et al. (1996) J. Biol. Chem. 271, 2929-2934]. The molecular nature of the membrane perturbation that precedes oxidative damage is still unknown. EPR spectra of spin probes incorporated in submitochondrial particles (SMP) and in model membranes suggest that Ca(2+)-cardiolipin (CL) complexation plays an important role. Ca(2+)-induced lipid domain formation was detected in SMP but not in mitoplasts, in SMP extracted lipids, or in CL-containing liposomes. The results were interpreted in terms of Ca2+ sequestration of CL tightly bound to membrane proteins, in particular the ADP-ATP carrier, and formation of CL-enriched strongly immobilized clusters in lipid shells next to boundary lipid. The in-plane lipid and protein rearrangement is suggested to cause increased reactive oxygen species production in succinate-supplemented, antimycin A-poisoned SMP, favoring the formation of carbon-centered radicals, detected by EPR spin trapping. Removal of tightly bound CL is also proposed to cause protein aggregation, facilitating intermolecular thiol oxidation. Lipid peroxidation was also monitored by the disappearance of the nitroxide EPR spectrum. The decay was faster for nitroxides in a more hydrophobic environment, and was inhibited by butylated hydroxytoluene, by EGTA, or by substituting Mg2+ for Ca2+. In addition, Ca2+ caused an increase in permeability, evidenced by the release of carboxyfluorescein from respiring SMP. The results strongly support Ca2+ binding to CL as one of the early steps in the molecular mechanism of Ca(2+)-induced nonspecific inner mitochondrial membrane permeabilization.
机译：线粒体的Ca2 +和P（i）积累触发许多变化，导致内膜通透性非特异性增加[Kowaltowski，A. J.，et al。 （1996）生物化学杂志。化学271，2929-2934]。在氧化损伤之前的膜扰动的分子性质仍然是未知的。 EPR谱掺入线粒体颗粒（SMP）和模型膜中的自旋探针的EPR谱表明Ca（2 +）-cardiolipin（CL）络合发挥重要作用。 Ca（2+）诱导的脂质结构域形成在SMP中检测到，但在丝裂质，SMP提取的脂质或含CL的脂质体中未检测到。用与膜蛋白紧密结合的CL的Ca2 +螯合，尤其是ADP-ATP载体，以及在边界脂质旁边的脂质壳中形成的富含CL的强固定簇来解释结果。平面内脂质和蛋白质的重排被认为会导致琥珀酸补充的抗霉素A中毒的SMP中活性氧种类的产生增加，这有助于通过EPR自旋捕获检测到以碳为中心的自由基的形成。还提出去除紧密结合的CL引起蛋白质聚集，从而促进分子间硫醇氧化。还通过一氧化氮EPR光谱的消失来监测脂质过氧化。在更疏水的环境中，对于氮氧化物而言，衰减更快，并且可通过丁基化羟基甲苯，EGTA或通过用Mg2 +代替Ca2 +来抑制。另外，Ca 2+引起通透性增加，这由呼吸SMP释放出的羧基荧光素所证明。结果强烈支持Ca2 +绑定到CL作为Ca（2+）诱导的非特异性内部线粒体膜通透性分子机制的早期步骤之一。

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