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MitoQ counteracts telomere shortening and elongates lifespan of fibroblasts under mild oxidative stress

MitoQ counteracts telomere shortening and elongates lifespan of fibroblasts under mild oxidative... Oxidative damage is thought to be a major causal factor for replicative senescence and human aging ( Harman, 1994 ). Leakage of superoxide from the mitochondrial respiratory chain is an important source of oxidative stress ( Raha & Robinson, 2000 ). Targeting antioxidants to mitochondria is an efficient way to attenuate oxidative damage in mitochondria due to the production of reactive oxygen species (ROS) in isolated mitochondria ( Kelso et al ., 2001 ; Echtay et al ., 2002 ) and in mitochondria within cells ( Kelso et al ., 2001 ; Hwang et al ., 2001 ). Therefore, by determining the effect of these antioxidants it should be possible to establish whether oxidative damage has a role in telomere shortening. It has been shown that selective targeting of a potent antioxidant to mitochondria is achieved by attaching the redox active moiety of ubiquinol to the decyltriphenylphosphonium (DPPT) cation, resulting in the mitochondria-specific antioxidant mitoQ [10-(6′-ubiquinonyl) decyltriphenylphosphonium bromide] ( Kelso et al ., 2001 ). Ubiquinol acts as an antioxidant by donating a hydrogen atom from one of its hydroxyl groups to a lipid peroxyl radical, which decreases lipid peroxidation within the mitochondrial inner membrane ( Ingold et http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Aging Cell Wiley

MitoQ counteracts telomere shortening and elongates lifespan of fibroblasts under mild oxidative stress

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References (23)

Publisher
Wiley
Copyright
© Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland 2003
ISSN
1474-9718
DOI
10.1046/j.1474-9728.2003.00040.x
pmid
12882327
Publisher site
See Article on Publisher Site

Abstract

Oxidative damage is thought to be a major causal factor for replicative senescence and human aging ( Harman, 1994 ). Leakage of superoxide from the mitochondrial respiratory chain is an important source of oxidative stress ( Raha & Robinson, 2000 ). Targeting antioxidants to mitochondria is an efficient way to attenuate oxidative damage in mitochondria due to the production of reactive oxygen species (ROS) in isolated mitochondria ( Kelso et al ., 2001 ; Echtay et al ., 2002 ) and in mitochondria within cells ( Kelso et al ., 2001 ; Hwang et al ., 2001 ). Therefore, by determining the effect of these antioxidants it should be possible to establish whether oxidative damage has a role in telomere shortening. It has been shown that selective targeting of a potent antioxidant to mitochondria is achieved by attaching the redox active moiety of ubiquinol to the decyltriphenylphosphonium (DPPT) cation, resulting in the mitochondria-specific antioxidant mitoQ [10-(6′-ubiquinonyl) decyltriphenylphosphonium bromide] ( Kelso et al ., 2001 ). Ubiquinol acts as an antioxidant by donating a hydrogen atom from one of its hydroxyl groups to a lipid peroxyl radical, which decreases lipid peroxidation within the mitochondrial inner membrane ( Ingold et

Journal

Aging Cell – Wiley

Published: Apr 1, 2003

Keywords: antioxidant; fibroblast; hyperoxia; mitoQ; oxidative stress; senescence; telomere

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