Triphenylphosphonium (TPP) derivatives are commonly used to target chemical into mitochondria. We show that alkyl-TPP cause reversible, dose- and hydrophobicity-dependent alterations of mitochondrial morphology and function and a selective decrease of mitochondrial inner membrane proteins including subunits of the respiratory chain complexes, as well as components of the mitochondrial calcium uniporter complex. The treatment with alkyl-TPP resulted in the cleavage of the pro-fusion and cristae organisation regulator Optic atrophy-1. The structural and functional effects of alkyl-TPP were found to be reversible and not merely due to loss of membrane potential. A similar effect was observed with the mitochondria-targeted antioxidant MitoQ.

中文翻译：

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亲脂性阳离子对线粒体内膜蛋白复合物的选择性和可逆破坏

三苯基膦 (TPP) 衍生物通常用于将化学物质靶向线粒体。我们表明，烷基-TPP 会引起线粒体形态和功能的可逆、剂量和疏水性依赖性改变，以及线粒体内膜蛋白（包括呼吸链复合物的亚基）以及线粒体钙单向转运蛋白复合物的成分的选择性减少。用烷基-TPP 处理导致促融合和嵴组织调节剂 Optic atrophy-1 的分裂。发现烷基-TPP 的结构和功能效应是可逆的，而不仅仅是由于膜电位的损失。线粒体靶向抗氧化剂 MitoQ 也观察到了类似的效果。