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大气PM_(2.5)对原代培养大鼠心肌细胞的毒性 被引量:20

Study on the Toxicity of Ambient PM2.5 to Primary Cultured Myocardial Cells of Neonatal Rats
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摘要 目的探讨PM2.5及其组分对原代培养大鼠心肌细胞的毒性及其剂量-反应关系。方法对出生24h的SD大鼠的乳鼠分离心肌细胞进行原代培养,以不同浓度(0.1、1.0、10.0、20.0、30.0、100.0、200.0μg/ml)的PM2.5全颗粒物及其水溶性提取物、有机提取物染毒24h,采用MTT法测定细胞的存活率,并观察染毒对心肌细胞搏动的影响。结果0.1、1.0、10.0μg/ml的全颗粒物、水溶性提取物和有机提取物染毒时,心肌细胞存活率均随染毒浓度升高而上升,在10.0μg/ml时达到最高,随后,随浓度的升高而降低;有机提取物的毒性明显高于水溶性提取物,心肌细胞的搏动频率随染毒浓度的升高而降低。结论以细胞存活率为指标,观察到PM2.5及其组分对心肌细胞的hormesis效应;PM2.5及其组分还可抑制心肌细胞的搏动频率并存在剂量-反应关系。 Objective To understand the ambient PM2.5 component and the toxicity to primary cultured myocardial cells of neonatal rats. Methods Primary myocardial cells cultures were prepared from 1-day-oM Sprague-Dawley rats and treated with PM2.5 suspension and its organic and water-soluble extracts at various concentrations for 24 h. The cellular viability was measured with MTT methods, and the beat of myocardial cells was observed and counted under inverted microscope. Results PM2.5 suspension and its organic and water-soluble extracts increased the viability of myocardial ceils at the concentrations bolow 10.0μg/ml, but above this, they could significantly decrease the viability of myocardial cells with a dose-dependent manner. The toxicity of organic extract of PM2.5 was significantly higher than that of water-soluble extract. PM2.5 suspension and its organic and water- soluble extracts also dose-dependently inhibited the beat frequencies of myocardial cells. Conclusion PM2.5 and its extracts show a hormesis effect on the cultured myocardial cells in the case of the cellular viability is taken as the response parameter. PM2.5 and its extracts can inhibit the beat of myocardial cells.
出处 《环境与健康杂志》 CAS CSCD 北大核心 2006年第1期17-20,共4页 Journal of Environment and Health
基金 国家自然科学基金资助项目(30230310 30571534)
关键词 空气污染 颗粒物 心肌细胞 Air pollution Particulate matter Myocardial cell
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参考文献17

  • 1Gold DR, Litonjua A, Schartz J, et al. Ambient pollution and heart rate variability[J]. Circulation, 2000, 101:1267-1273.
  • 2Magari SR, Hauser R, Schwartz J, et al. Association of heart rate variability with occupational and environmental exposure to particulate air pollution[J]. Circulation, 2001, 104:986-991.
  • 3Peters A, Liu E, Verrier RL, et al. Increased particulate air pollution and the triggering of myocardial infarction[J]. Circulation, 2001303:2810-2815.
  • 4Michael R, Wayne E, Caseio TRG, et al. Particulate matter exposure in cars is associated with cardiovascular effects in healthy young men[J].Am J Respir Criti Care Med, 2004,169: 934-940.
  • 5Douglas WD. Epidemiologic evidence of cardiovascular effects of particulate air pollution[J]. Environ Health Perspeet, 2001, 109:483-486.
  • 6Lucas MN. Fine particulate matter and cardiovascular disease[J]. Fuel Processing Technology, 2000, 65-66: 55-67.
  • 7Vincent R, Kumarathasan P, Goegan P, et al. Inhalation toxicology of urban ambient particulate matter:acute cardiovascular effects in rats[J]. Res Rep Health Eff Inst, 2001, 104: 5-62.
  • 8William PW, Matthew JC, Julianne PN, et al.Cardiovascular and systemic responses to inhaled pollutants in rodents: effects of ozone and particulate matter[J]. Environ Health Perspect, 2001,109: 539-546.
  • 9Gordon T, Nadziejko C, Schhsinger R, et al. Pulmonary and cardiovascular effects of acute exposure to concentrated ambient particulate matter in rats [J]. Toxicol Lett, 1998, 96-97:285-288.
  • 10Kang YJ, Li Y, Zhou Z, Roberts AM, et al. Elevation of serum endothelins and cardiotoxicity induced by particulate matter (PM2.5) in rats with acute myocardial infarction [J]. Cardiovasc Toxicol,2002, 2: 253-262.

二级参考文献10

  • 1SalemHarry.Toxicology of low- level exposure:evidence forhormesis[].Journal of Applied Toxicology.2000
  • 2CavieresM F,JaegerJ,W Porter.Developmental toxicity of acommercial herbicide mixture in mice:I.Effects on embryo im-plantation and litter size[].EnvironmentalH ealthPerspectives.2002
  • 3StebbingA R D.Hormesis:interpreting theβ- curve using con-trol theory[].Journal of Applied Toxicology.2000
  • 4CalabreseE J,BaldwinL A.Evidence that hormesis repre-sents an"overcompensation"response to a disruption in home-ostasis[].Ecotoxicology andEnvironmentalSafety.1999
  • 5MorréD J.Chemical hormesis in cell growth:a moleculartargetat the cell surface[].Journal of Applied Toxicology.2000
  • 6Stebbing A R D.Tolerance and hormesis-increased resistance to copper in hydroids linked to hormesis[].Marine Environmental Research.2002
  • 7Stebbing A R D.Growth hormesis : a by-product of control[].Health Physics.1987
  • 8Stebbing ADR.Hormesis-the stimulation of growth by low levels of inhibitors[].Science of the Total Environment.1982
  • 9Calabrese E J and Baldwin L A.Chemical hormesis: it’ s historical foundations as a biological hypothesis[].Toxicologic Pathology.1999
  • 10Calabrese E J and Baldwin L A.The marginalization of hormesis[].Toxicologic Pathology.1999

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