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Oxidation and age-related macular degeneration: insights from molecular biology

Published online by Cambridge University Press:  20 October 2010

Sam Khandhadia
Affiliation:
Clinical Neurosciences Division, School of Medicine, University of Southampton, UK.
Andrew Lotery*
Affiliation:
Clinical Neurosciences Division, School of Medicine, University of Southampton, UK. Southampton General Hospital, Southampton, UK.
*
*Corresponding author: Andrew Lotery, Administrative Office, LD74, Clinical Neurosciences, South Lab & Path Block, Southampton General Hospital, Southampton SO16 6YD, UK. E-mail: a.j.lotery@soton.ac.uk

Abstract

Age-related macular degeneration (AMD) is the leading cause of blindness in the developed world. It is a multifactorial disease, and current therapy predominantly limits damage only when it has already occurred. The macula is a source of high metabolic activity, and is therefore exposed to correspondingly high levels of reactive oxygen species (ROS). With age, the balance between production of ROS and local antioxidant levels is shifted, and damage ensues. Systemic ROS and antioxidant levels in AMD reflect these local processes. Genetic studies investigating mutations in antioxidant genes in AMD are inconclusive and further studies are indicated, especially to determine the role of mitochondria. Oral antioxidant supplements could be beneficial, and diet modification may help. Future treatments might either increase antioxidant capacity or reduce the production of ROS, using methods such as genetic manipulation. This article reviews the role of oxidative stress in AMD and the potential therapies that might have a role in preventing the blindness resulting from this disease.

Type
Review Article
Copyright
Copyright © Cambridge University Press 2010

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References

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Further reading, resources and contacts

Swaroop, A. et al. (2009) Unraveling a multifactorial late-onset disease: from genetic susceptibility to disease mechanisms for age-related macular degeneration. Annual Review of Genomics and Human Genetics 10, 19-43Google Scholar
Muller, F.L. et al. (2007) Trends in oxidative aging theories. Free Radical Biology and Medicine 43, 477-503Google Scholar
Brennan, L.A. and Kantorow, M. (2009) Mitochondrial function and redox control in the aging eye: role of MsrA and other repair systems in cataract and macular degenerations. Experimental Eye Research 88, 195-203Google Scholar
Boulton, M. et al. (2001) Retinal photodamage. Journal of Photochemistry and Photobiology B 64, 144-161Google Scholar
Cai, J. et al. (2000) Oxidative damage and protection of the RPE. [Review] [138 refs]. Progress in Retinal and Eye Research 19, 205-221Google Scholar
Online Mendelian Inheritance in Man (OMIM) is a comprehensive database of gene-specific information:http://www.ncbi.nlm.nih.gov/omimGoogle Scholar
A database of current clinical trials can be found at:http://www.clinicaltrials.govGoogle Scholar
Swaroop, A. et al. (2009) Unraveling a multifactorial late-onset disease: from genetic susceptibility to disease mechanisms for age-related macular degeneration. Annual Review of Genomics and Human Genetics 10, 19-43Google Scholar
Muller, F.L. et al. (2007) Trends in oxidative aging theories. Free Radical Biology and Medicine 43, 477-503Google Scholar
Brennan, L.A. and Kantorow, M. (2009) Mitochondrial function and redox control in the aging eye: role of MsrA and other repair systems in cataract and macular degenerations. Experimental Eye Research 88, 195-203Google Scholar
Boulton, M. et al. (2001) Retinal photodamage. Journal of Photochemistry and Photobiology B 64, 144-161Google Scholar
Cai, J. et al. (2000) Oxidative damage and protection of the RPE. [Review] [138 refs]. Progress in Retinal and Eye Research 19, 205-221Google Scholar
Online Mendelian Inheritance in Man (OMIM) is a comprehensive database of gene-specific information:http://www.ncbi.nlm.nih.gov/omimGoogle Scholar
A database of current clinical trials can be found at:http://www.clinicaltrials.govGoogle Scholar