期刊文献+

氯乙烯职业暴露与DNA加合物εdA、εdC水平表达相关性研究 被引量:1

Study of Expression Correlation between Levels of DNA Adducts and Occupational Exposure to Vinyl Chloride
下载PDF
导出
摘要 目的研究氯乙烯职业接触人群的DNA损伤情况。方法以氯乙烯车间工人为暴露组,行政管理和后勤人员为对照组。每位研究对象采集4 mL静脉血全血,运用超高效液相串联质谱检测研究对象血样中εdA、εdC两种DNA加合物的含量,应用单因素方差和多因素方差分析性别、年龄、饮酒、吸烟、氯乙烯暴露情况等因素对εdA和εdC含量的影响。结果暴露组血样中εdA、εdC的含量分别为:(3.38±2.58) pmol/mg,(2.37±1.84) pmol/mg;对照组血样中εdA、εdC的含量分别为:(1.39±1.20) pmol/mg,(0.83±0.73) pmol/mg,氯乙烯暴露组血样中εdA和εdC水平均高于对照组的水平差异有统计学意义(P<0.05)。年龄、吸烟、饮酒对研究对象血样中εdA含量的影响差异无统计学意义(P> 0.05)。年龄、吸烟对研究对象血样中εdC含量的影响差异无统计学意义(P> 0.05),饮酒者血样中εdC含量高于非饮酒者,差异具有统计学意义(P<0.05)。结论氯乙烯职业暴露水平低于我国职业接触限值(PC-TWA为10 mg/m^3)的剂量水平时,暴露组的εdA和εdC含量显著高于对照组的水平。即低暴露水平的氯乙烯也可引起DNA加合物的增加,导致DNA损伤,增加了接触者的患癌风险。 Objectives To assess the DNA damage of occupational population exposed to vinyl chloride. Methods The exposure group consisted workers from the vinyl chloride plant. The control group consisted administration management and service personnel. A 4 mL whole blood of venous blood sample was obtained from each participant. An ultra-performance liquid chromatography tandem mass spectrometry was used to detect two kinds of DNA adducts,εdA and εdC, in blood samples of participants. One-way ANOVA and Multi-way ANOVA were used to analyze the effect of gender, age, drinking, smoking, and vinyl chloride exposure on εdA and εdC content in blood. Results The contents of εdA and εdC in blood sample of exposure group were(3.38±2.58) pmol/mg and(2.37±1.84) pmol/mg, respectively. The contents of εdA and εdC in blood sample of control group were(1.39±1.20) pmol/mg and(0.83±0.73) pmol/mg, respectively. The levels of εdA and εdC in the exposure group were higher than the levels in the control group with significant differences(P<0.05). There was no significant difference in the effects of age, smoking, and drinking on the content of εdA in blood sample of participants(P>0.05). Similarly, there was no significant difference in the effects of age and smoking on the content of εdC in the blood sample of participants(P > 0.05). The level of εdC in blood sample of drinkers was higher than that of non-drinkers with significant differences(P < 0.05). Conclusions Even if the level of occupational exposure to vinyl chloride is lower than the occupational exposure limit(PC-TWA=10 mg/m^3), the level of εdA and εdC in the blood of exposure group was significantly higher than that of the control group. The low level of vinyl chloride exposure can also cause the increase of DNA adducts, resulting in DNA damage, and increasing the cancer risk to contact person.
作者 崔师伟 刘晓东 潘兴富 闫慧芳 CUI Shiwei;LIU Xiaodong;PAN Xingfu;YAN Huifang
出处 《环境卫生学杂志》 2019年第2期108-112,共5页 JOURNAL OF ENVIRONMENTAL HYGIENE
基金 国家科技支撑计划项目(2014BAI12B02)
关键词 氯乙烯 DNA加合物 DNA损伤 εdA εdC vinyl chloride DNA adducts DNA damage εdA εdC
  • 相关文献

参考文献3

二级参考文献93

  • 1MALTONI C, LEFEMINE G, CHIECO P, et al. Vinyl chloride carcinogenesis : current results and perspectives [ J ]. Med Lay, 1974,65 (11/12) :421 -444.
  • 2BLOCK J B. Angiosarcoma of the liver following vinyl chloride exposure[J]. JAMA ,1974,229( 1 ) :53 -54.
  • 3CLEWELL H J,GENTRY P R,GEARHART J M,et al. Comparison of cancer risk estimates for vinyl chloride using animal and human data with a PBPK model [ J ]. Sci Total Environ,2001,274 (1 -3 ) :37 - 66.
  • 4CHIANG S Y, SWENBERG J A,WEISMAN W H,et al. Mutagenicity of vinyl chloride and its reactive metabolites, chloroethylene oxide and chloroacetaldehyde, in a metabolically competent human B-lymphoblastoid line[J]. Carcinogenesis, 1997,18( 1 ) :31 -36.
  • 5BARBIN A. Role of etheno DNA adducts in carcinogenesis induced by vinyl chloride in rats [ J ]. IARC Sci Publ, 1999,150 : 303 - 313.
  • 6SCHERER E, WINTERWERP H, EMMELOT P. Modification of DNA and metabolism of ethyl carbamate in vivo: formation of 7-(2-oxoethyl) guanine and its sensitive determination by reductive tritiation using 3H-sodium borohydride [J]. IARC Sci Publ, 1985 ,70:109 -125.
  • 7BARBIN A,LAIB R J, BARTSCH H. Lack of miscoding properties of 7-(2-oxoethyl) guanine, the major vinyl chloride-DNA adduct [ J ]. Cancer Res,1985, 45(6) :2440 -2444.
  • 8LEVINE R L,YANG L Y,HOSSAIN M,et al. Mutagenesis induced by a single 1, N6-ehenodeoxyadenosine adduct in human cells[ J]. Cancer Res, 2000,60(15) :4098 -4104.
  • 9SPEINA E, KIERZEK A M, TUDEK B. Chemical rearrangement and repair pathways of 1, N6-ethenoadenine[ J]. Mutat Res, 2003,531 ( 1/ 2) : 205 -217.
  • 10PETRONZELLI F, RICCIO A, MARKHAM G D,et al. Investigation of the substrate spectrum of the human mismatch-specific DNA N-glycosylase MED1 (MBD4) : fundamental role of the catalytic domain [ J ]. Cell Physiol,2000,185 (3) :473 - 480.

共引文献5

同被引文献6

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部