N-Acetyltransferase 2 Phenotype May Be Associated with Susceptibility to Age-Related Cataract
Free radicals and oxidative damage play roles in aging and age-related ocular diseases such as cataracts, so defensive mechanisms become important factors for protection. Because N-acetylation is involved in a wide variety of detoxification processes, this study was conducted to examine the relation...
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Published in | Current eye research Vol. 30; no. 10; pp. 835 - 839 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Informa UK Ltd
01.10.2005
Taylor & Francis |
Subjects | |
Online Access | Get full text |
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Summary: | Free radicals and oxidative damage play roles in aging and age-related ocular diseases such as cataracts, so defensive mechanisms become important factors for protection. Because N-acetylation is involved in a wide variety of detoxification processes, this study was conducted to examine the relationship between the acetylator phenotypes and genotypes in a group of patients with age-related cataract. Sixty-one cases of age-related cataract and 104 controls were included in this study. Blood was collected in EDTA-containing tubes, and genomic DNA was extracted from the white blood cells by high pure PCR template preparation kit. Genotyping of NAT2 polymorphisms were detected by using a LightCycler-NAT2 mutation detection kit in real-time PCR. There was a significant difference in the distribution of the NAT2*6A acetylator phenotype between cases and the controls. The odds ratio of cataract for the NAT2*6A slow phenotype was 3.8 (95% CI = 1.08 to 13.11, p = 0.032) compared with the fast type. Our results suggest that slow acetylators are at higher risk of developing age-related cataracts than fast acetylators. As NAT2 is an important xenobiotic-metabolizing enzyme and theoretically xenobiotics such as ultraviolet B radiation, smoking, and alcohol use may induce cataract formation, NAT2 gene polymorphisms may be associated with genetic susceptibility of cataract. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0271-3683 1460-2202 |
DOI: | 10.1080/02713680591003799 |