Deleterious consequences of antioxidant supplementation on lifespan in a wild-derived mammal

While oxidative damage owing to reactive oxygen species (ROS) often increases with advancing age and is associated with many age-related diseases, its causative role in ageing is controversial. In particular, studies that have attempted to modulate ROS-induced damage, either upwards or downwards, us...

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Published inBiology letters (2005) Vol. 9; no. 4; p. 20130432
Main Authors Selman, Colin, McLaren, Jane S., Collins, Andrew R., Duthie, Garry G., Speakman, John R.
Format Journal Article
LanguageEnglish
Published England The Royal Society 23.08.2013
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Summary:While oxidative damage owing to reactive oxygen species (ROS) often increases with advancing age and is associated with many age-related diseases, its causative role in ageing is controversial. In particular, studies that have attempted to modulate ROS-induced damage, either upwards or downwards, using antioxidant or genetic approaches, generally do not show a predictable effect on lifespan. Here, we investigated whether dietary supplementation with either vitamin E (α-tocopherol) or vitamin C (ascorbic acid) affected oxidative damage and lifespan in short-tailed field voles, Microtus agrestis. We predicted that antioxidant supplementation would reduce ROS-induced oxidative damage and increase lifespan relative to unsupplemented controls. Antioxidant supplementation for nine months reduced hepatic lipid peroxidation, but DNA oxidative damage to hepatocytes and lymphocytes was unaffected. Surprisingly, antioxidant supplementation significantly shortened lifespan in voles maintained under both cold (7 ± 2°C) and warm (22 ± 2°C) conditions. These data further question the predictions of free-radical theory of ageing and critically, given our previous research in mice, indicate that similar levels of antioxidants can induce widely different interspecific effects on lifespan.
Bibliography:Present address: Institute of Biodiversity, Animal Health and Comparative Medicine, University of Glasgow, Glasgow, G12 8QQ, UK.
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Present address: Division of Orthopaedic and Accident Surgery, Queen's Medical Centre, University of Nottingham, Nottingham NG7 2UH, UK.
Present address: Department of Nutrition, School of Medicine, University of Oslo, PO Box 1046 Blindern, 0316 Oslo, Norway.
ISSN:1744-9561
1744-957X
DOI:10.1098/rsbl.2013.0432