Red wine consumption is inversely associated with 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine-DNA adduct levels in prostate.
Red wine consumption is inversely associated with 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine-DNA adduct levels in prostate.
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DOI：
10.1158/1940-6207.capr-11-0100
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发表时间：
2011-10
期刊：
影响因子：
--
通讯作者：
Tang D
中科院分区：
文献类型：
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作者：
Rybicki BA;Neslund-Dudas C;Bock CH;Nock NL;Rundle A;Jankowski M;Levin AM;Beebe-Dimmer J;Savera AT;Takahashi S;Shirai T;Tang D
在人类中，遗传变异和饮食因素可能会改变暴露于2-氨基-1-甲基-6-苯基咪唑[4，5-B]吡啶（PhIP）的生物效应，PhIP是高温烹饪肉类产生的主要杂环胺之一，通过形成DNA加合物具有致癌潜力。以前，我们报道了烤红肉消费与人前列腺中PhIP-DNA加合物水平相关。在本研究中，我们扩大了我们的调查，以估计391例前列腺癌病例的饮料消费和前列腺中PhIP-DNA加合物水平之间的关联。在分析的15种饮料中，红葡萄酒消费与PhIP-DNA加合物水平的相关性最强，在肿瘤（p=0.006）和非肿瘤（p=0.002）前列腺细胞中均显示出负相关性。非裔美国人和白色人的红葡萄酒消费量有显著差异，但前列腺中的PhIP-DNA加合物水平并不因种族而异。然而，与白人相比，在非洲裔美国人中，红葡萄酒消费与PhIP-DNA加合物水平之间的关联不如与特定（例如，SULT 1A 1和UGT 1A 10基因型）和非特异性（例如，非洲血统）遗传变异。在一个多变量模型中，红葡萄酒消费的协变量解释了两个种族群体前列腺中PhIP-DNA加合物水平变化的可比百分比（13-16%），但上述遗传因素解释了非裔美国人病例中33%的PhIP-DNA加合物变化，而白人中仅19%的PhIPDNA加合物变化。我们的结论是，红葡萄酒的消费可能会抵消PhIP暴露在人类前列腺的生物效应，但遗传因素可能发挥更大的作用，特别是在非洲裔美国人。
In humans, genetic variation and dietary factors may alter the biologic effects of exposure to 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), one of the major heterocyclic amines generated from cooking meats at high temperatures that has carcinogenic potential through the formation of DNA adducts. Previously, we reported grilled red meat consumption associated with PhIP-DNA adduct levels in human prostate. In the present study, we expanded our investigation to estimate the associations between beverage consumption and PhIP-DNA adduct levels in prostate for 391 prostate cancer cases. Of the 15 beverages analyzed, red wine consumption had the strongest association with PhIP-DNA adduct levels showing an inverse correlation in both tumor (p=0.006) and non-tumor (p=0.002) prostate cells. Red wine consumption differed significantly between African-American and white cases, but PhIP-DNA adduct levels in prostate did not vary by race. In African Americans compared with whites, however, associations between red wine consumption and PhIP-DNA adduct levels were not as strong as associations with specific (e.g., SULT1A1 and UGT1A10 genotypes) and non-specific (e.g., African ancestry) genetic variation. In a multivariable model, the covariate for red wine consumption explained a comparable percentage (13-16%) of the variation in PhIP-DNA adduct levels in prostate across the two racial groups, but the aforementioned genetic factors explained 33% of the PhIP-DNA adduct variation in African-American cases, while only 19% of the PhIPDNA adduct variation in whites. We conclude that red wine consumption may counteract biologic effects of PhIP exposure in human prostate, but genetic factors may play an even larger role, particularly in African Americans.