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首页> 外文期刊>Molecular and Cellular Biology >Mitochondrial Lipid Abnormality and Electron Transport Chain Impairment in Mice Lacking α-Synuclein
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Mitochondrial Lipid Abnormality and Electron Transport Chain Impairment in Mice Lacking α-Synuclein

机译：缺乏α-突触核蛋白的小鼠线粒体脂质异常和电子转运链受损。

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The presynaptic protein α-synuclein, implicated in Parkinson disease (PD), binds phospholipids and has a role in brain fatty acid (FA) metabolism. In mice lacking α-synuclein (Snca?/?), total brain steady-state mass of the mitochondria-specific phospholipid, cardiolipin, is reduced 22% and its acyl side chains show a 51% increase in saturated FAs and a 25% reduction in essential n-6, but not n-3, polyunsaturated FAs. Additionally, 23% reduction in phosphatidylglycerol content, the immediate biosynthetic precursor of cardiolipin, was observed without alterations in the content of other brain phospholipids. Consistent with these changes, more ordered lipid head group and acyl chain packing with enhanced rotational motion of diphenylhexatriene (DPH) about its long axis were demonstrated in time-resolved DPH fluorescence lifetime experiments. These abnormalities in mitochondrial membrane properties were associated with a 15% reduction in linked complex I/III activity of the electron transport chain, without reductions in mitochondrial number, complex II/III activity, or individual complex I, II, III, or IV activity. Reduced complex I activity is thought to be a critical factor in the development of PD. Thus, altered membrane composition and structure and impaired complex I/III function in Snca?/? brain suggest a relationship between α-synuclein's role in brain lipid metabolism, mitochondrial function, and PD.
机译：突触前蛋白α-突触核蛋白与帕金森病（PD）有关，与磷脂结合并在脑脂肪酸（FA）代谢中起作用。在缺乏α-突触核蛋白（ Snca ？/？）的小鼠中，线粒体特异性磷脂心磷脂的总脑稳态质量降低了22％，且其酰基侧链显示饱和脂肪酸增加51％，基本 n -6（而不是 n -3）多不饱和脂肪酸减少25％。另外，观察到磷脂酰甘油含量（心磷脂的直接生物合成前体）降低了23％，而其他脑磷脂的含量没有变化。与这些变化相一致，在时间分辨的DPH荧光寿命实验中，二苯基己三烯（DPH）绕其长轴旋转运动增强，脂头基团和酰基链堆积更加有序。线粒体膜特性的这些异常与电子传输链的相连复合物I / III活性降低15％相关，而线粒体数，复合物II / III活性或单个复合物I，II，III或IV活性未降低。复杂的I活性降低被认为是PD发生的关键因素。因此， Snca ？/？大脑中膜成分和结构的改变以及复杂的I / III功能受损提示α-突触核蛋白在脑脂质代谢中的作用，线粒体功能，和PD。

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