期刊文献+

沥青烟致小鼠肺损伤及细胞周期改变的研究

Experimental study on lung injury and cell cycle changes in mice induced by bitumen fume
原文传递
导出
摘要 目的研究沥青烟致癌和致突变作用的机制。方法用沥青烟对小鼠进行不同剂量(55、165 mg/m^3)和不同时间(30、60 d)的染毒,观察小鼠肺组织病理形态改变,并用流式细胞仪进行小鼠肺组织细胞DNA含量的检测和细胞周期的分析。结果随着沥青烟染毒时间和剂量的增加,小鼠肺组织病变表现为不同程度的不典型增生和原位癌;同时小鼠肺组织细胞各周期指数发生变化,G_1期细胞数下降,S期阻滞,进入G_2/M期的细胞减少,细胞增殖指数(PI)增加,异倍体指数(DI)升高,与对照组比较,差异均有统计学意义(P<0.05)。染毒相同时间时,55 mg/m^3和165mg/m^3剂量组的PI均高于对照组,165 mg/m^3剂量组的DI高于55mg/m^3剂量组,差异均有统计学意义(P<0.05或P<0.01)。相同染毒剂量下,60 d处理组的DI[(1.16±1.51)×10^(-2)、(1.20±2.30)×10^(-2)]均高于30 d处理组[(1.14±0.88)×10^(-2)、(1.16±1.47)×10^(-2)],差异有统计学意义(P<0.05)。结论沥青烟所致小鼠肺组织产生的癌前病变可能与细胞周期的改变有关。 Objective To investigate the carcinogenic and mutagenic mechanism of bitumen fume. Methods The experimental mice were forced to inhale the bitumen fume at different exposure level(55 mg/m^3, 165 mg/m^3) and in different time(30 days,60 days). The pathological changes of the lung tissue in mice were observed with H. E staining. The content of the DNA in the lung tissue of mice and the cell circles were determined with flow cytometry. Results The lesion of the lung tissue in mice comprised the atypical hyperplasia of different levels and the carcinoma in situ with the increase of the containment time and dosage;the cycle index was changed: the number of the G 1 phase cells was decreased, the S phase was retarded, the cells entering the G 2/S phase were decreased,the cell proliferation index(PI) was increased and the heteroploid DNA index(DI) was increased( P 〈 0. 05) .The cell index in the 55 mg/m^3 group and the 165 mg/m^3 group was higher than that in the control group when the containment time was same. The heteroploid DNA index(DI) in the 55 mg/m^3 group was significantly higher than that in the 165 mg/m^3 group(P 〈 0.05 or P 〈0.01).When the containment dosage was same,the DI in the 60 days treatment group( 1.16 ± 1.51 × 10^-2, 1.20 ± 2.3 × 10^-2 ) was all significantly higher than those in the 30 daystreatmentgroup(1.14±8.8×10^-2,1.16±1.47×10^-2)(P〈0.05). Conclusion The precancerous lesion in the lung tissue of the mice induced by the bitumen fume may be related with the changes of the cell cycle.
出处 《中华劳动卫生职业病杂志》 CAS CSCD 北大核心 2006年第7期406-408,共3页 Chinese Journal of Industrial Hygiene and Occupational Diseases
基金 甘肃省科学技术厅科学事业费资助项目(QS041-C33-27)
关键词 烃类 流式细胞术 细胞周期 Hydrocarbons Flow cytometry Lung Cell cycle
  • 相关文献

参考文献12

  • 1King RW,Puzinauskas VP,Holdsworth CE,et al.Asphalt composition and health effects:a critical review.Technical Publication,Washington DC:American Petroleum institute,1984.1-11.
  • 2Boffetta P,Burstyn I.Study of carcinogencity of bitumen fume in humans.Am J Ind Med,2003,43:1-2.
  • 3褚连富,孙培莲,满瑛,王永进.铝电解工人恶性肿瘤流行病学研究[J].中华劳动卫生职业病杂志,1996,14(6):347-350. 被引量:7
  • 4彭仁和,李凤英,辛业志,田国彬,许支农.沥青作业工人癌症回顾性队列研究[J].实用预防医学,1999,6(1):61-62. 被引量:2
  • 5Partanen T,Boffetta P,Heikkila PR,et al.Cancer risk for European asphalt workers.Scand J Work Environ Health.1995,21:252-258.
  • 6Heikkila PR,Vaananen V,Hameila M,et al.Mutagenicity of bitumen and asphalt fume.Toxicol In Vitro,2003,17:403-412.
  • 7Zhao HW,Yin XJ,Frazer D,et al.Effects of paving asphalt fume exposure on genotoxic and mutagenic activities in the rat lung.Mutat Res,2004,557:137-149.
  • 8Toraason M,Hayden C,Marlow D,et al.DNA strand breaks,oxidative damage,and 1-OH pyrene in roofers with coal-tar pitch dust and/or asphalt fume exposure.Int Arch Occup Environ Health,2001,74:396-404.
  • 9Schoket B,Hewer A,Grover PL,et al.Covalent binding of components of coal tar,creosote and bitumen to the DNA of the skin and lungs of mice following topical application.Carcinogenesis,1988,9:1253-1258.
  • 10张鋆歆.肺癌前病变[J].国外医学(肿瘤学分册),2003,30(3):208-210. 被引量:3

二级参考文献32

  • 1全国油毡行业流行病学调查协作组,巩德田,杨淑芹,刘金凤,洪瑾.油毡工人癌症死亡率的研究[J].工业卫生与职业病,1993,19(6):338-341. 被引量:6
  • 2杜保田.职业卫生与安全百科全书[M].北京:中国大百科全书出版社,1987.727-883.
  • 3张跃东 赵子辰 等.吉林省沥青作业工人恶性肿瘤死亡十一年回顾调查与病因探讨[J].中华劳动卫生职业病杂志,1986,4(4):223-223.
  • 4Chyezewski L, Nildinski J, Chyczewska E, et al. Morphological aspects of carcinogene.sis in the lung[J]. Lung Cancer, 2001 , (Suppl2) :S17-25.
  • 5Mori M, Rao SK, Popper HH, et al. Atypical adenomatous hyperplasia of the lung: a probable forerunner in the development of adenocarcinoma of the lung[J]. Mod Pathol , 2001 ,14(2) :72-84.
  • 6Nishisaka T, Takeshima Y, Inai K, et al. Evaluation of p53 gene mutation and loos of heterozygosity of 3p, 9p and 17p in precancerous lesions of 29 lung cancer patients[J]. Hiroshima J Med Sci, 2000 ,4.9(2) : 109-116.
  • 7Lonardo F, Rusch V, Langenfeld J, et al. Overexpression of cyclins D1 and E is frequent in bronchial preneoplasia and precedes squamous cell carcinoma development[J ]. Cancer Res , 1999 , 59( 10 ) : 2470-2476.
  • 8George PJ. Fluorescence bronchoscopy for the early detection of lung cancer[J]. Thorax , 1999,54(2) :180-183.
  • 9Venmans BJ, van Boxem TJ, Smit EF, et al. Outcome of bronchial carcirmma in situ[J]. Chest , 2000 , 117(6) : 1572-1576.
  • 10Sanz Ortega J, Saez MC, Sierra E, et al. 3p21, 5q21, and9p21 allelic deletions are frequently found in normal bronchial cells adjacent to non-small-cell lung cancer, while they are unusual in patients with no evidence of malignancy[J]. J Pathol,2001 , 195(4) :429-434.

共引文献8

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