Mitochondrial targeting of quinones: Therapeutic implications

被引:113
作者
Cocheme, 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.
机构
[1] MRC, Dunn Human Nutr Unit, Cambridge CB2 2XY, England
[2] Univ Otago, Dept Chem, Dunedin, New Zealand
[3] Univ Otago, Dept Biochem, Dunedin, New Zealand
基金
英国医学研究理事会;
关键词
mitochondria; antioxidants; MitoQ; BIOMEMBRANE-PRODUCED ENERGY; OXIDOREDUCTASE COMPLEX-I; PERFUSED RAT HEARTS; OXIDATIVE-PHOSPHORYLATION; RESPIRATORY-CHAIN; SKELETAL-MUSCLE; COENZYME Q(10); PROTON LEAK; SUPEROXIDE-PRODUCTION; ANTIOXIDANT DEFENSE;
D O I
10.1016/j.mito.2007.02.007
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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. (c) 2007 Elsevier B.V. and Mitochondria Research Society. All rights reserved.
引用
收藏
页码:S94 / S102
页数:9
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