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目的通过对外周血淋巴细胞DNA损伤程度和人8羟-基鸟嘌呤DNA糖苷酶(hum an8-oxoguan ine DNA glycosydase,hOGG1)基因多态性的研究,了解石棉肺与DNA损伤和hOGG1基因型的关系。方法以101名石棉作业工人作为观察组、141名非石棉作业工人作为对照组进行了流行病学调查。利用彗星试验检测DNA损伤程度;用多聚酶链反应-限制性片段长度多态性(polym erasechain reaction-restricted fragm ents length polymorph ism,PCR-RELP)法确定hOGG1基因Ser326Cys多态分布。结果(1)石棉接触组基础DNA损伤程度(basal DNA dam age,DB,34.8±16.8)、H2O2诱导后的DNA损伤程度(H2O2-induced DNA dam age,DH,136.7±36.0)及修复损伤4 h后的DNA损伤程度(repair DNA dam age,DR,51.0±18.7)均显著高于对照组(P<0.01)。石棉肺组DH(147.0±30.8)和DR(56.9±21.4)显著高于非石棉肺组(125.7±38.2和44.9±15.4)(P<0.01)。(2)石棉接触组和对照组hOGG1基因Ser326Cys多态分布差异没有统计学意义(χ2=0.22,P=0.89)。而石棉接触组中,石棉肺人群Ser/Ser、Ser/Cys、Cys/Cys基因型分布频率分别为25.5%、51.0%和23.5%,与非石棉肺人群(48.0%、36.0%和16.0%)间差异有统计学意义(χ2=6.023,P<0.05)。石棉肺组中Ser/Cys和Cys/Cys基因型人群,DH和DR均高于非石棉肺组相应人群(P<0.05)。(3)在校正了年龄、性别、吸烟和饮酒等因素后,hOGG1基因型对患石棉肺的风险无明显影响(OR=0.66;95%CI=0.38~1.13)。结论接触石棉会导致DNA损伤,携带Cys等位基因的人群DNA对H2O2氧化损伤敏感性增强且DNA损伤的修复能力降低可能是促成石棉肺的原因之一。
OBJECTIVE: To study the DNA damage of human peripheral blood lymphocytes and the polymorphism of human humoral-8-oxoguanine DNA glycosydase (hOGG1) gene, so as to understand the relationship between DNA damage and hOGG1 genotype relationship. Methods A total of 101 asbestos workers were employed as observation group and 141 non-asbestos workers as control group for epidemiological investigation. The degree of DNA damage was detected by comet assay. The polymorphism of Ser326Cys in hOGG1 gene was determined by polymerase chain reaction-restricted fragments length polymorphism (PCR-RELP). Results (1) Basal DNA dam age (DB, 34.8 ± 16.8), H2O2-induced DNA dam age (DH, 136.7 ± 36.0) The DNA damage (DR, 51.0 ± 18.7) was significantly higher than that of the control group (P <0.01). DH (147.0 ± 30.8) and DR (56.9 ± 21.4) in asbestosis group were significantly higher than those in non-asbestos lung group (125.7 ± 38.2 and 44.9 ± 15.4, P <0.01). (2) The polymorphism of Ser326Cys in hOGG1 gene in asbestos exposure group and control group was not statistically different (χ2 = 0.22, P = 0.89). In the asbestos exposure group, the frequencies of Ser / Ser, Ser / Cys and Cys / Cys genotypes were 25.5%, 51.0% and 23.5% respectively in asbestosis lungs, and were significantly higher than those in non-asbestosis lungs (48.0%, 36.0% and 16.0% The difference was statistically significant (χ2 = 6.023, P <0.05). The population of Ser / Cys and Cys / Cys genotypes in asbestosis group were higher than those in non-asbestosis group (P <0.05). (3) The hOGG1 genotype had no significant effect on the risk of asbestos lung (OR = 0.66; 95% CI = 0.38-1.13) after adjusting for age, gender, smoking and alcohol consumption. Conclusions Exposure to asbestos causes DNA damage, and susceptibility to oxidative DNA damage in humans carrying the Cys allele is enhanced and reduced DNA damage repair may contribute to asbestosis in lungs.