Dagli Rushabh J, Kulkarni Suhas, Duraiswamy Prabu, Dagli Namrata R, Khara Nimit V, Khara Birva N
Department of Public Health Dentistry, Vyas Dental College & Hospital, Jodhpur, Rajasthan, India.
J Int Oral Health. 2013 Aug;5(4):62-7. Epub 2013 Aug 28.
There is increasing evidence that a major part of the tumour-promoting action of alcohol is mediated via its first, toxic and carcinogenic metabolite acetaldehyde.
MATERIALS & METHODS: The double blinded randomized control trial was designed for 82 male volunteers aged 20-29 years. Exclusion criteria were individual under antibiotic therapy, smokers, mutant Aldehyde Dehydrogenase deficient subject or any other systemic disease. Subjects were randomized in experimental (alcohol + soft drink) and control group (soft drink) from each pair of equal body weighted volunteers. The amount of alcohol consumed was calculated to be equivalent to 0.7 g alcohol/kilogram of body weight. Samples of breath for Acetaldehyde concentration (AC) were captured with the aid of a highly reproducible fuel cell gas-sampling device (PST-M1; Lions Laboratories, Cardiff, Wales). In Statistical analysis, mean AC was compared among both groups at different interval using paired t-test and Analysis of variance.
Mean acetaldehyde level was recorded higher ([Formula: see text]) among interventional group which can be produced from ethanol during metabolism or by oro-pharyngeal microbes. After 15 minutes of drink, the AC was [Formula: see text] in ethanol group compared to [Formula: see text] in soft-drink group. There was significant increase in AC after 1 hour ([Formula: see text]) which was [Formula: see text] in ethanol group compared to [Formula: see text] in soft-drink group.
Although acetaldehyde is metabolite of alcohol, its organ specific production with risk for oro-pharyngeal and pulmonary carcinogenesis makes alcohol an independent risk factor of carcinogenesis. How to cite this article: Dagli RJ, Kulkarni S, Duraiswamy P, Dagli NR, Khara NV, Khara BN. Is Alcohol an independent risk factor for Oro-Pharyngeal and Pulmonary Carcinogenesis - An Acetaldehyde concentrations based Double Blinded Randomized Control Trial. J Int Oral Health 2013; 5(4):62-67.
越来越多的证据表明,酒精促进肿瘤发生的主要作用是通过其第一种有毒且致癌的代谢产物乙醛介导的。
该双盲随机对照试验针对82名年龄在20至29岁之间的男性志愿者设计。排除标准包括正在接受抗生素治疗的个体、吸烟者、乙醛脱氢酶突变缺陷受试者或任何其他全身性疾病患者。从每对体重相等的志愿者中,将受试者随机分为实验组(酒精+软饮料)和对照组(软饮料)。计算得出摄入的酒精量相当于每千克体重0.7克酒精。借助高度可重复的燃料电池气体采样装置(PST-M1;Lions Laboratories,加的夫,威尔士)采集用于检测乙醛浓度(AC)的呼气样本。在统计分析中,使用配对t检验和方差分析在不同时间间隔比较两组的平均AC。
记录到干预组的平均乙醛水平较高([公式:见原文]),这可能是乙醇在代谢过程中或由口咽微生物产生的。饮用后15分钟,乙醇组的AC为[公式:见原文],而软饮料组为[公式:见原文]。1小时后AC显著升高([公式:见原文]),乙醇组为[公式:见原文],软饮料组为[公式:见原文]。
尽管乙醛是酒精的代谢产物,但其在特定器官的产生以及对口咽和肺癌发生的风险使得酒精成为致癌的独立危险因素。如何引用本文:Dagli RJ,Kulkarni S,Duraiswamy P,Dagli NR,Khara NV,Khara BN。酒精是口咽和肺癌发生的独立危险因素吗——一项基于乙醛浓度的双盲随机对照试验。《国际口腔健康杂志》2013年;5(4):62 - 67。