期刊文献+

苯及其代谢产物在小鼠骨髓中形成DNA加合物的实验研究 被引量:6

D N Aadduct formation in the bone m arrow of mice treated with benzene and some metabolites
原文传递
导出
摘要 目的 观察苯及其主要代谢产物苯酚、氢醌、苯醌及苯酚和氢醌联合染毒在小鼠骨髓中形成的 D N A 加合物及其髓性毒性。方法 改进的32 P 后标记方法。结果 苯及其主要代谢产物均能在小鼠骨髓细胞中形成至少1 种 D N A 加合物,相对加合物水平从0 .85 ×10 - 8 ~6 .78 ×10 - 8 不等。骨髓细胞计数结果表明:单独染苯酚或氢醌,对小鼠骨髓细胞均没有抑制作用,但二者联合染毒对小鼠却表现出增强的髓性毒作用。结论 苯及其主要代谢产物均能在小鼠骨髓细胞中形成 D N A 加合物,苯的代谢产物形成的 D N A 加合物与髓性毒性有关。 Objective To investigate D N Aadduct formation induced by benzene and some metabolitesin the bone marro w and the m yelotoxicity . Methods Female Kun ming mice were treated intraperioneallywith benzene and some metabolites twice daily ,and nuclease P1 enhanced 32 P postlabelling assay was used tostudy the effect . Results No adduct was detected in the bone marrow of control group . At least one major D N A adduct was detected in the bone marrow of mice treated with benzene ,phenol,hydroquinone ,benzo quinone respectively and coadministration of phenol and hydroquinone . The relative adduct levels ranged from0 .85 ×10 - 8 ~6 .78 ×10 - 8 . Ad ministration of phenol(75 m g/kg) or hydroquinone (75 m g/kg) twice dailyfor 12 days did not result in a suppression of bone m arrow cellularity respectively . However ,the conco mitantad ministration of phenol(75 m g/kg) and hydroquinone(50 m g/kg) twice a day for 12 days produced a signif icant decrease in bone m arrow cellularity . Conclusion Benzene and some metabolites showed myelotoxicityby forming adductin the bone marro w .
出处 《中华劳动卫生职业病杂志》 CAS CSCD 1999年第4期196-199,共4页 Chinese Journal of Industrial Hygiene and Occupational Diseases
关键词 代谢产物 ^32P后标记方法 DNA加合物 Benzene Metabolites 32 P postlabelling D N Aadduct Myelotoxicity
  • 相关文献

参考文献11

二级参考文献15

  • 1王春光,李桂兰,尹松年.苯代谢产物DNA加合物形成特性研究[J].中华预防医学杂志,1994,28(5):297-298. 被引量:8
  • 2顾祖维,黄雷鸣.职业人群遗传毒性效应的监测[J].工业卫生与职业病,1990,16(1):16-21. 被引量:8
  • 3王春光,中华预防医学杂志,1993年,27卷,344页
  • 4李桂兰,Environ Health Perspect,1996年,104卷,1337页
  • 5常平,中华预防医学杂志,1996年,30卷,111页
  • 6Fang J L,Carcinogenesis,1995年,16卷,2177页
  • 7李桂兰,卫生研究,1995年,24卷,260页
  • 8李桂兰,卫生研究,1995年,24卷,特辑,3页
  • 9王春光,中华预防医学杂志,1994年,28卷,297页
  • 10王春光,中华预防医学杂志,1993年,27卷,344页

共引文献25

同被引文献56

  • 1耿月华,刘雨,汪晓媛.聊城市干洗业职业危害调查[J].中国城乡企业卫生,2004(1):16-16. 被引量:1
  • 2夏昭林,孙品,张忠彬,金锡鹏.苯的职业健康危害研究的回顾与展望[J].中华劳动卫生职业病杂志,2005,23(4):241-243. 被引量:92
  • 3唐焕文,梁海荣,庄志雄,何云.低剂量氢醌诱导hPARP-1蛋白正常及缺陷细胞适应性反应研究[J].中华劳动卫生职业病杂志,2005,23(4):274-277. 被引量:4
  • 4李桂兰,尹午山,尹松年.苯DNA加合物的组织分布及其与细胞遗传毒性的关系[J].卫生研究,1995,24(5):260-262. 被引量:9
  • 5王英.我国有机溶剂职业中毒现状与防治对策[J].职业与健康,2007,23(15):1341-1342. 被引量:7
  • 6[1]Decaprio AP.The toxicology of hydroquinone relevance to occupational and environmental exposure[J].Crit Rev Toxicol,1999,29:283-330.
  • 7[3]Lindsey RH Jr,Bender RP,Osheroff N.Effects of benzene metabolites on DNA cleavage mediated by human topoisomerase Ⅱ alpha:1,4-hydroquinone is a topoisomerase Ⅱ poison[J].Chem Res Toxicol,2005,18:761-770.
  • 8[4]Bironaite D,Siegel D,Moran JL,et al.Stimulation of endothelial IL-8 (Eil-8) prodction and apoptosis by phenolic metabolites of benzene in HL-60 cells and human bone marrow endothelial cells[J].Chem Biol Interact,2004,149:177-188.
  • 9[7]Gaskell M,McLuckie KI,Farmer PB.Comparison of the mutagenic activity of the benzene metabolites,hydroquinone and parabenzoquinone in the supF forward mutation assay:a role for minor DNA adducts formed from hydroquinone in benzene mutagenicity[J].Mutat Res,2004,554:387-398.
  • 10[8]Gaskell M,McLuckie KI,Farmer PB.Comparison of the repair of DNA damage induced by the benzene metabolites hydroquinone and p-benzoquinone:a role for hydroquinone in benzene genotoxicity[J].Carcinogenesis,2005,26:673-680.

引证文献6

二级引证文献16

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