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Study of Correlation between Smoking and DNA Damage from Peasants Living in Mengjin County, Luoyang

Author: XieHuiLing
Tutor: ZhangQiao
School: Zhengzhou University
Course: Health Toxicology
Keywords: Smoke DNA damage Single - cell gel electrophoresis assay Micronucleus test
CLC: R114
Type: Master's thesis
Year: 2011
Downloads: 59
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Abstract

Smoking can cause lung cancer, laryngeal, pharyngeal cancer and other tumors. But today, people smoking carcinogenic mechanism is not yet very clear. DNA as the genetic material of the organism, its damage is considered to be one of the important mechanisms of tumorigenesis. Some studies have shown that the smoking smoke contains large amounts of free radicals, free radicals can cause DNA damage directly caused DNA breaks induce gene mutations and cell cancerous. The purpose of this study selected Mengjin County of Luoyang healthy male non-smokers and smokers, DNA damage indicators and chromosome damage in peripheral blood lymphocytes by measuring related to smoking and non-smoking crowd, to explore the relationship of smoking and DNA damage, for further study smoking carcinogenic mechanism for the accumulation of information. The method of cluster sampling selected from Luoyang Mengjin County are investigating the the villages health of male villagers as the object of study. Group 2 the research object serum cotinine content detected by ELISA (enzyme-linked immunosorbent assay, ELISA), plasma 8 - hydroxy-deoxyguanosine (8-hydroxydeoxygunosine ,8-OHdG) content and plasma polycyclic aromatics DNA adducts (polycyclic aromatic hydrocarbon-DNA, PAH-DNA) adducts levels; alkaline single-cell gel electrophoresis assay (single cell gel electrophoresis, SCGE) trace whole blood assay study DNA single strand breaks; using blood lymphocyte cytokinesis block method micronucleus test (by cytokinesis-block micronucleus assay in human lymphocyte cytokinesis - block micronucleus) detection study of peripheral blood lymphocyte micronucleus rate. The comparative study of various indicators are grouped according to the date of smoking and smoked. 1 GENERAL INFORMATION: The study included 114 patients. Smoking group 67 cases, with an average 53.406 ± 7.061 years; 47 cases of non-smoking group, an average of 51.312 ± 10.481 years old, the age groups showed no statistical significance (P gt; 0.05); each age, smoking and non-smoking group between body mass index (Body Mass Index, BMI) differences were not statistically significant (P gt; 0.05), indicating that the smoking group and the non-smoking group balanced comparable. 2 cotinine results: no-smoking group may cotinine content and age linear correlation was not statistically significant (r = 0.183, P = 0.218); compared with the non-smoking group (4.661 ± 4 ± 1.802 ng/m1) smoking group significantly higher cotinine content (327.011 ± 4 ± 1.293 ng / ml, P lt; 0.05); smoking group smoked and cotinine content linear correlation (r = 0.815, P = 0.021) ; lt; 20 cigarettes / d smoking group, ≥ 20 cigarettes / d smoking group cotinine content was significantly higher (P lt; 0.05), cotinine content was positively correlated with the number of cigarettes smoked daily. 3. Genetic toxicity test results: The Pearson correlation analysis showed that non-smokers comet tail length, comet tail with age linear correlation was not statistically significant (comet tail length: r = 0.279, P = 0.089; comet tail rate : r = 0.268, P = 0.093); compared with nonsmokers (comet tail length: 10.903 ± 1.891μm; comet tail rate: 18 .. 550 ± 1.471%), tail length of the smoking group (28.161 ± 4.572 μm) and comet tail (34.402 ± 5.491%) was significantly higher (P lt; 0.05); smoking group smoked tail length and comet tail rate linear correlation (comet tail length: r = 0.772, P = 0.001; the comet tail rate: r = 0.811, P = 0.001); lt; 20 cigarettes / d smoking group ≥ 20 cigarettes / d-smoking group comet tail length and comet tailing was significantly higher (P lt; 0.05), the comet tail length and comet the trailing rate and the number of cigarettes smoked per day was positively correlated. The micronucleus rate among quartiles range of 5-10% o, median 8% o. Smoking group (median 10 ‰, P25 = 9 ‰, P75 = 11 ‰) was significantly higher in the micronucleus rate compared to the non-smoking group (median 5% o P25 = 3 ‰, P75 = 6 ‰) (W = 1128.500, P lt; 0.05); lt; 20 cigarettes / d, and ≥ 20 cigarettes / d2 group micronucleus rate there is no difference (W = 1204, P = 0.491 gt; 0.05). But different smoked the micronucleus rate differences among the three groups was statistically significant (chi-square statistic of 30.701, P lt; 0.05); With the increase of age smoke, the micronucleus rate was significantly higher (P lt; 0.05) . 4.DNA adduct detection results: non-smokers 8-OHdG and PAH-DNA content and age MA no statistically significant correlation (8-OHdG: r = 0.232, P = 0.107; PAH-DNA: r = 0.124 , P = 0.115); 8-OHdG non-smoking group (1.612 ± 0.510) ng / ml; PAH-DNA (63.022 ± 6.360) ng / ml compared to smoking group 8-OHdG (3.912 ± 0.461) ng / ml ng / ml and PAH-DNA content (96.811 ± 4.882) was significantly higher (P lt; 0.05); the the smoking group PAH-DNA smoked linear correlation (r = 0.702, P = 0.001), but 8-OHdG smoked linear correlation was not statistically significant (r = 0.204, P = 0.097); lt; 20 cigarettes / d smoking group, ≥ 20 cigarettes / d-smoking group of 8-OHdG and PAH-DNA content was significantly liter high (P lt; 0.05), 8-OHdG and PAH-DNA content and the number of cigarettes smoked per day was positively correlated. Conclusion Smoking can cause human peripheral blood lymphocyte DNA single-strand breaks and chromosomal damage caused genotoxic effects; smoking can induce cell DNA adduct 8-OHdG and the increase of PAH-DNA, DNA damage effects that smoking has, is induced one of the important mutagens human genetic material injury.

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