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APE1基因和ADPRT基因多态与慢性苯中毒易感性的关系
引用本文:孙品,张忠彬,万俊香,金锡鹏,夏昭林. APE1基因和ADPRT基因多态与慢性苯中毒易感性的关系[J]. 中华劳动卫生职业病杂志, 2006, 24(7): 385-389
作者姓名:孙品  张忠彬  万俊香  金锡鹏  夏昭林
作者单位:200032,上海,复旦大学公共卫生学院劳动卫生教研室
基金项目:国家自然科学基金资助项目(30271113);国家“973”项目(2002CB512902)
摘    要:目的探讨脱嘌呤/脱嘧啶核酸内切酶(APEl)和腺苷酸二磷酸核糖基转移酶(APDRT)的基因多态与慢性苯中毒易感性的关系.方法采用病例对照研究,以152名苯中毒工人为病例组,152名接触苯而无中毒表现的工人为对照组.应用创造酶切位点的限制性片断长度多态检测技术(CRS-RFLP)检测APE1基因Asp148Glu位点和ADPRT基因Val762Ala位点的多态性.结果APE1 Asp148Glu多态与ADPRT Val762Ala多态的各基因型在病例组和对照组的分布差异无统计学意义(P>0.05);携带APE1 Asp148Glu Asp/Asp基因型的饮酒个体比携带该基因型的不饮酒个体发生慢性苯中毒的危险性升高(OR=4.13,95% CI:1.07~15.85,P=0.03);多因素Logistic回归分析提示,吸烟对慢性苯中毒发病风险具有一定的修饰作用(OR=0.33,95% CI:0.14~0.75,P=0.01).结论APE1 Asp148Glu和ADPRT Val762Ala位点多态与慢性苯中毒的发病风险没有关系.饮酒与APE1 Asp148Glu多态可能存在联合作用,仍需进一步研究确定.

关 键 词:苯中毒 脱嘌呤/脱嘧啶核酸内切酶 腺苷酸二磷酸核糖基转移酶 基因多态性
收稿时间:2005-06-17
修稿时间:2005-06-17

Relationship of genetic polymorphism in APE 1 and ADPRT to risks of chronic benzene poisoning
SUN Pin,ZHANG Zhong-bin,WAN Jun-xiang,JIN Xi-peng,XIA Zhao-lin. Relationship of genetic polymorphism in APE 1 and ADPRT to risks of chronic benzene poisoning[J]. Chinese journal of industrial hygiene and occupational diseases, 2006, 24(7): 385-389
Authors:SUN Pin  ZHANG Zhong-bin  WAN Jun-xiang  JIN Xi-peng  XIA Zhao-lin
Affiliation:Department of Oocupational Health, School of Public Health, Fudan University. Shanghai 200032, China
Abstract:OBJECTIVE: To explore the relationship between genetic polymorphisms in apurinic/apyrimidinic endonuclease (APE1) and ADP ribosyltransferase (ADPRT) and individuals' susceptibility to chronic benzene poison ing (BP). METHODS: A case-control study was conducted. One hundred and fifty-two B P patients and 152 workers occupationally exposed to benzene without poisoning manifestations were investigated. The mismatched bases combined to create restriction site with restrained fragment length polymorphism technique (CRS-RFLP) was used for detecting the single nucleotide polymorphisms (SNPs) at Asp148Glu of APE1 gene and Val762Ala of ADPRT gene. RESULTS: There was no significant difference in the distribution of genotypes of APE1Asp148Glu and ADPRTVal762Ala between the patients and the control groups. Compared with individuals having genotype of APE1Asp148Glu T/T without habit of alcohol consumption, there was a 4.13 times increased risk of BP for the alcohol user with genotype of APE1Asp148Glu T/T (OR = 4.13, 95% CI: 1.07 - 15.85, P = 0.03). The analysis of Logistic regression showed that smoking may play some role in modifying the risk of cironic benzene poisoning (OR = 0.33, 95% CI: 0.14 - 0.75, P = 0.01). CONCLUSION: The genetic polymorphisms in APE1Asp148Glu, ADPRTVal762Ala are not related to the risk of BP. Potential interaction is found between alcohol consumption and polymorphism of APE1Asp148Glu. Further study is needed to elucidate this interaction.
Keywords:Benzene poisoning  APE1  ADPRT  Genetic polymorphism
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