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      Oxidative Damage and the Prevention of Age-Related Cataracts

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          Abstract

          Purpose: Cataracts are often considered to be an unavoidable consequence of aging. Oxidative damage is a major cause or consequence of cortical and nuclear cataracts, the most common types of age-related cataracts. Methods: In this review, we consider the different risk factors, natural history and etiology of each of the 3 major types of age-related cataract, as well as the potential sources of oxidative injury to the lens and the mechanisms that protect against these insults. The evidence linking different oxidative stresses to the different types of cataracts is critically evaluated. Results: We conclude from this analysis that the evidence for a causal role of oxidation is strong for nuclear, but substantially lower for cortical and posterior subcapsular cataracts. The preponderance of evidence suggests that exposure to increased levels of molecular oxygen accelerates the age-related opacification of the lens nucleus, leading to nuclear cataract. Factors in the eye that maintain low oxygen partial pressure around the lens are, therefore, important in protecting the lens from nuclear cataract. Conclusions: Maintaining or restoring the low oxygen partial pressure around that lens should decrease or prevent nuclear cataracts.

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          Causes and prevalence of visual impairment among adults in the United States.

          Nathan Congdon, Benita J O'Colmain, Caroline C. W. Klaver … (2004)
          To estimate the cause-specific prevalence and distribution of blindness and low vision in the United States by age, race/ethnicity, and gender, and to estimate the change in these prevalence figures over the next 20 years. Summary prevalence estimates of blindness (both according to the US definition of < or =6/60 [< or =20/200] best-corrected visual acuity in the better-seeing eye and the World Health Organization standard of < 6/120 [< 20/400]) and low vision (< 6/12 [< 20/40] best-corrected vision in the better-seeing eye) were prepared separately for black, Hispanic, and white persons in 5-year age intervals starting at 40 years. The estimated prevalences were based on recent population-based studies in the United States, Australia, and Europe. These estimates were applied to 2000 US Census data, and to projected US population figures for 2020, to estimate the number of Americans with visual impairment. Cause-specific prevalences of blindness and low vision were also estimated for the different racial/ethnic groups. Based on demographics from the 2000 US Census, an estimated 937 000 (0.78%) Americans older than 40 years were blind (US definition). An additional 2.4 million Americans (1.98%) had low vision. The leading cause of blindness among white persons was age-related macular degeneration (54.4% of the cases), while among black persons, cataract and glaucoma accounted for more than 60% of blindness. Cataract was the leading cause of low vision, responsible for approximately 50% of bilateral vision worse than 6/12 (20/40) among white, black, and Hispanic persons. The number of blind persons in the US is projected to increase by 70% to 1.6 million by 2020, with a similar rise projected for low vision. Blindness or low vision affects approximately 1 in 28 Americans older than 40 years. The specific causes of visual impairment, and especially blindness, vary greatly by race/ethnicity. The prevalence of visual disabilities will increase markedly during the next 20 years, owing largely to the aging of the US population.
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            Age-related nuclear cataract-oxidation is the key.

            Roger J. W. Truscott (2005)
            Age is by far the biggest risk factor for cataract, and it is sometimes assumed that cataract is simply an amplification of this aging process. This appears not to be the case, since the lens changes associated with aging and cataract are distinct. Oxidation is the hallmark of age-related nuclear (ARN) cataract. Loss of protein sulfhydryl groups, and the oxidation of methionine residues, are progressive and increase as the cataract worsens until >90% of cysteine and half the methionine residues are oxidised in the most advanced form. By contrast, there may be no significant oxidation of proteins in the centre of the lens with advancing age, even past age 80. The key factor in preventing oxidation seems to be the concentration of nuclear glutathione (GSH). Provided that nuclear GSH levels can be maintained above 2 mm, it appears that significant protein oxidation and posttranslational modification by reactive small molecules, such as ascorbate or UV filter degradation products, is not observed. Adequate coupling of the metabolically-active cortex, the source of antioxidants such as GSH, to the quiescent nucleus, is crucial especially since it would appear that the cortex remains viable in old lenses, and even possibly in ARN cataract lenses. Therefore it is vital to understand the reason for the onset of the lens barrier. This barrier, which becomes apparent in middle age, acts to impede the flow of small molecules between the cortex and the nucleus. The barrier, rather than nuclear compaction (which is not observed in human lenses), may contribute to the lowered concentration of GSH in the lens nucleus after middle age. By extending the residence time within the lens centre, the barrier also facilitates the decomposition of intrinsically unstable metabolites and may exacerbate the formation of H(2)O(2) in the nucleus. This hypothesis, which is based on the generation of reactive oxygen species and reactive molecules within the nucleus itself, shifts the focus away from theories for cataract that postulated a primary role for oxidants generated outside of the lens. Unfortunately, due to marked variability in the lenses of different species, there appears at present to be no ideal animal model system for studying human ARN cataract.
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              Effect of ultraviolet radiation on cataract formation.

              Salvador Muñoz, Jessica S. West, Bridget Emmett … (1988)
              To investigate the relation of ultraviolet radiation and cataract formation, we undertook an epidemiologic survey of 838 watermen (mean age, 53 years) who worked on Chesapeake Bay. The annual ocular exposure was calculated from the age of 16 for each waterman by combining a detailed occupational history with laboratory and field measurements of sun exposure. Cataracts were graded by ophthalmologic examination for both type and severity. Some degree of cortical cataract was found in 111 of the watermen (13 percent), and some degree of nuclear cataract in 229 (27 percent). Logistic regression analysis showed that high cumulative levels of ultraviolet B exposure significantly increased the risk of cortical cataract (regression coefficient, 0.70; P = 0.04). A doubling of cumulative exposure increased the risk of cortical cataract by a factor of 1.60 (95 percent confidence interval, 1.01 to 2.64). Those whose annual average exposure was in the upper quartile had a risk increased by 3.30 (confidence interval, 0.90 to 9.97) as compared with those in the lowest quartile. Analysis using a serially additive expected-dose model showed that watermen with cortical lens opacities had a 21 percent higher average annual exposure to ultraviolet B (t-test, 2.23; P = 0.03). No association was found between nuclear cataracts and ultraviolet B exposure or between cataracts and ultraviolet A exposure. We conclude that there is an association between exposure to ultraviolet B radiation and cataract formation, which supports the need for ocular protection from ultraviolet B.
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                Author and article information

                Journal
                Journal ID (publisher-id): ORE
                Journal ID (nlm-ta): Ophthalmic Res
                Journal ID (doi): 10.1159/issn.0030-3747
                Title: Ophthalmic Research
                Publisher: S. Karger AG
                ISBN: 978-3-8055-9574-2
                ISBN: 978-3-8055-9575-9
                ISSN (Print): 0030-3747
                ISSN (Electronic): 1423-0259
                Publication date Subscription-year: 2010
                Publication date (Print): September 2010
                Publication date (Electronic): 09 September 2010
                Volume: 44
                Issue: 3
                Pages: 155-165
                Affiliations
                Departments of aOphthalmology and Visual Sciences and bCell Biology and Physiology, Washington University, and cBarnes Retina Institute, Saint Louis, Mo., USA
                Author notes
                *Prof. David C. Beebe, PhD, Department of Ophthalmology and Visual Sciences, Washington University, Campus Box 8096, 660 S. Euclid Avenue, Saint Louis, MO 63110 (USA), E-Mail beebe@wustl.edu
                Article
                Publisher ID: 316481 Pmcid ID: PMC2952186 Other ID: Ophthalmic Res 2010;44:155–165
                DOI: 10.1159/000316481
                PMC ID: PMC2952186
                PubMed ID: 20829639
                SO-VID: c78e4f63-5460-4ce5-9072-38cf96c1a702
                Copyright © © 2010 S. Karger AG, Basel
                License:

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                History
                Page count
                Figures: 2, Pages: 11
                Categories
                Subject: Paper

                ScienceOpen disciplines: Vision sciences,Ophthalmology & Optometry,Pathology
                Keywords: Oxidative damage,Age-related cataract
                Data availability:
                ScienceOpen disciplines: Vision sciences, Ophthalmology & Optometry, Pathology
                Keywords: Oxidative damage, Age-related cataract

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