Mitochondrial oxidative damage contributes to a range of degenerative diseases. Consequently, the selective inhibition of mitochondrial oxidative damage is a promising therapeutic strategy. One way to do this is to invent antioxidants that are selectively accumulated into mitochondria within patients. Such mitochondria-targeted antioxidants have been developed by conjugating the lipophilic triphenylphosphonium cation to an antioxidant moiety, such as ubiquinol or alpha-tocopherol. These compounds pass easily through all biological membranes, including the blood-brain barrier, and into muscle cells and thus reach those tissues most affected by mitochondrial oxidative damage. Furthermore, because of their positive charge they are accumulated several-hundredfold within mitochondria driven by the membrane potential, enhancing the protection of mitochondria from oxidative damage. These compounds protect mitochondria from damage following oral delivery and may therefore form the basis for mitochondria-protective therapies. Here we review the background and work to date on this class of mitochondria-targeted antioxidants.

中文翻译：

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通过与亲脂性阳离子结合将抗氧化剂靶向线粒体。

线粒体氧化损伤会导致一系列退行性疾病。因此，选择性抑制线粒体氧化损伤是一种很有前途的治疗策略。做到这一点的一种方法是发明抗氧化剂，这些抗氧化剂可以选择性地积累到患者体内的线粒体中。此类靶向线粒体的抗氧化剂已通过将亲脂性三苯基鏻阳离子与抗氧化剂部分（例如泛醇或α-生育酚）缀合而开发。这些化合物很容易通过所有生物膜，包括血脑屏障，进入肌肉细胞，从而到达受线粒体氧化损伤影响最大的组织。此外，由于它们的正电荷，它们在膜电位的驱动下在线粒体内积累了数百倍，增强保护线粒体免受氧化损伤。这些化合物在口服给药后保护线粒体免受损伤，因此可能构成线粒体保护疗法的基础。在这里，我们回顾了这类线粒体靶向抗氧化剂的背景和迄今为止的工作。