کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
9910131 1548651 2005 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Green tea consumption, genetic susceptibility, PAH-rich smoky coal, and the risk of lung cancer
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی تحقیقات سرطان
پیش نمایش صفحه اول مقاله
Green tea consumption, genetic susceptibility, PAH-rich smoky coal, and the risk of lung cancer
چکیده انگلیسی
Experimental evidence suggests that green tea (Camellia sinesis) may reduce the risk of lung cancer through several hypothesized mechanisms including scavenging oxidative radicals, inhibition of tumor initiation, and modulation of detoxification enzymes. However, epidemiologic results have not been consistent as to the relationship between green tea consumption and lung caner prevention. We employed a population-based case-control study of 122 cases and 122 controls to investigate the effect that green tea consumption may have on the risk of lung cancer and whether polymorphisms in 8-oxoguanine-DNA glycosylase (OGG1), glutathione-S-transferase M1 (GSTM1), and aldo-keto reductase 1C3 (AKR1C3) modify such an association. Daily green tea consumption was associated with a non-significant reduction in lung cancer risk. However, the effect of smoky coal exposure was higher for non-drinkers (odds ratio (OR) = 4.93; 95% confidence interval (95% CI) = 1.27-19.13) than for drinkers (OR = 1.88; 95% CI = 1.01-3.48). Further, among individuals with the OGG1 Cys326 allele, daily consumption was associated with a 72% reduction (95% CI = 0.09-0.94). Among GSTM1 null homozygotes, those who consumed green tea daily had a non-significant reduction in risk compared with non-consumers. Green tea consumption had no effect among OGG1 Ser326 homozygotes or GSTM1 carriers. In addition, AKR1C3 genotype did not modulate the effect of green tea consumption. The chemopreventive effects of green tea in this population may be restricted to individuals who are particularly susceptible to oxidative stress and oxidative DNA damage.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Mutation Research/Genetic Toxicology and Environmental Mutagenesis - Volume 582, Issues 1–2, 4 April 2005, Pages 53-60
نویسندگان
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