Cochemé Helena M, Kelso Geoffrey F, James Andrew M, Ross Meredith F, Trnka Jan, Mahendiran Thabo, Asin-Cayuela Jordi, Blaikie Frances H, Manas Abdul-Rahman B, Porteous Carolyn M, Adlam Victoria J, Smith Robin A J, Murphy Michael P
MRC Dunn Human Nutrition Unit, Wellcome Trust/MRC Building, Hills Road, Cambridge CB2 2XY, UK.
Mitochondrion. 2007 Jun;7 Suppl:S94-102. doi: 10.1016/j.mito.2007.02.007. Epub 2007 Mar 16.
Mitochondrial oxidative damage contributes to a range of degenerative diseases. Ubiquinones have been shown to protect mitochondria from oxidative damage, but only a small proportion of externally administered ubiquinone is taken up by mitochondria. Conjugation of the lipophilic triphenylphosphonium cation to a ubiquinone moiety has produced a compound, MitoQ, which accumulates selectively into mitochondria. MitoQ passes easily through all biological membranes and, because of its positive charge, is accumulated several hundred-fold within mitochondria driven by the mitochondrial membrane potential. MitoQ protects mitochondria against oxidative damage in vitro and following oral delivery, and may therefore form the basis for mitochondria-protective therapies.
线粒体氧化损伤会导致一系列退行性疾病。已有研究表明，泛醌可保护线粒体免受氧化损伤，但外部给予的泛醌只有一小部分会被线粒体摄取。将亲脂性三苯基膦阳离子与泛醌部分结合产生了一种化合物，即线粒体泛醌（MitoQ），它能选择性地积聚在线粒体内。MitoQ能轻易穿过所有生物膜，并且由于其正电荷，在线粒体膜电位的驱动下，它在线粒体内的积累量会增加数百倍。MitoQ在体外和口服给药后均可保护线粒体免受氧化损伤，因此可能构成线粒体保护疗法的基础。
