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Mol Metab. 2013 Sep 27;2(4):480-90. doi: 10.1016/j.molmet.2013.09.004. eCollection 2013.

Coenzyme Q10 prevents accelerated cardiac aging in a rat model of poor maternal nutrition and accelerated postnatal growth.

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1
University of Cambridge, Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Wellcome Trust - MRC Institute of Metabolic Science, Level 4, Box 289, Addenbrooke's Treatment Centre, Addenbrooke's Hospital, Cambridge CB2 OQQ, UK.

Abstract

Studies in human and animals have demonstrated that nutritionally induced low birth-weight followed by rapid postnatal growth increases the risk of metabolic syndrome and cardiovascular disease. Although the mechanisms underlying such nutritional programming are not clearly defined, increased oxidative-stress leading to accelerated cellular aging has been proposed to play an important role. Using an established rodent model of low birth-weight and catch-up growth, we show here that post-weaning dietary supplementation with coenzyme Q10, a key component of the electron transport chain and a potent antioxidant rescued many of the detrimental effects of nutritional programming on cardiac aging. This included a reduction in nitrosative and oxidative-stress, telomere shortening, DNA damage, cellular senescence and apoptosis. These findings demonstrate the potential for postnatal antioxidant intervention to reverse deleterious phenotypes of developmental programming and therefore provide insight into a potential translatable therapy to prevent cardiovascular disease in at risk humans.

KEYWORDS:

3-NT, 3-nitrotyrosine; 4-HNE, 4-hydroxynonenal; BER, base excision repair; Bax, Bcl2-associated protein; CAST, computer assisted stereology toolbox.; CVD, cardiovascular disease; Cellular senescence; CoQ, coenzyme Q; CuZnSOD, copper-zinc superoxide dismutase; DIG, dioxygenin; DNA damage; Developmental programming; ETC, electron transport chain; GPx, glutathione peroxidase; GR, glutathione reductase; MnSOD, manganese superoxide dismutase; NEIL1, nei endonuclease VIII-like 1; NOX, nicotinamide adenine dinucleotide diphosphate oxidase; NTHL1, Nthl endonuclease III like-1; O2, superoxide anion; OGG-1, 8 oxoguanine DNA glycosylase 1; OH-, hydroxy radicals; Oxidative-stress; PGFE, pulsed field gel electrophoresis; PRDX, peroxidiredoxin; RIS, reactive inflammatory species; RNS, reactive nitrogen species; ROS, reactive oxidative species; Telomere length; Ubiquinone; XO, xanthine oxidase; acta1, sarco endoplasmic reticulum Ca(2+) ATPase; actin, alpha-1; nppa, natriuretic peptide A; nppb, natriuretic peptide B; serca2, single strand breaks, SSBs

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