纳米颗粒物呼吸暴露致心血管系统损伤的硝化应激作用及可能机制
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摘要
纳米材料和大气颗粒物对环境与健康的影响是公众关注的焦点,也是生物医学领域的研究热点。纳米颗粒物主要是指粒径在100 nm以下的粒子,包括人工合成的纳米材料(1~100 nm)和自然环境中的空气动力学直径在100 nm以下的超细颗粒物。硝化应激(nitrosative stress)指机体对活性氮簇(reactive nitrogen species,RNS)的高应激性,主要表现为病理过程中过氧亚硝基阴离子(peroxynitrite,ONOO~-)过量生成,从而诱发细胞内蛋白质酪氨酸硝基化等,并最终导致细胞损伤。纳米颗粒物呼吸暴露诱导心血管系统损伤过程中,硝化应激稳态失衡与纳米颗粒穿透气血屏障进入血液循环密切关联,通过减少ONOO~-生成和清除过多的ONOO~-来拮抗硝化应激损伤将有可能成为防治空气颗粒物污染诱导心血管疾病发生发展的策略之一。
The influence of nanomaterials and atmospheric particles on environment and human health is a public focus, and it is also the hot spot in biomedical field. Nanoparticles(NPs) is the particles that the size is less than 100 nm, including synthetic nanomaterials(1-100 nm) and air ultrafine particles(UFPs). Reactive nitrogen species(RNS)are major mediators of nitrosative stress,which cause protein tyrosine nitration and subsequently facilitates the breakdown of the highly-structured cellular machinery as well as the damage of cell. This review focus on peroxynitrite(ONOO~-)-mediated nitrosative stress signaling,which is closely associated with endothelial cell injury and cardiovascular damage by penetrating air-blood carrier to blood circulation after nanoparticles exposure through breathing. Growing evidences indicate that targeting nitrosative stress may be an important strategy to prevent the cardiovascular diseases associated with air particles pollution.
The influence of nanomaterials and atmospheric particles on environment and human health is a public focus, and it is also the hot spot in biomedical field. Nanoparticles(NPs) is the particles that the size is less than 100 nm, including synthetic nanomaterials(1-100 nm) and air ultrafine particles(UFPs). Reactive nitrogen species(RNS)are major mediators of nitrosative stress,which cause protein tyrosine nitration and subsequently facilitates the breakdown of the highly-structured cellular machinery as well as the damage of cell. This review focus on peroxynitrite(ONOO~-)-mediated nitrosative stress signaling,which is closely associated with endothelial cell injury and cardiovascular damage by penetrating air-blood carrier to blood circulation after nanoparticles exposure through breathing. Growing evidences indicate that targeting nitrosative stress may be an important strategy to prevent the cardiovascular diseases associated with air particles pollution.
引文
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[28]王媛媛.硝化应激在心血管疾病中作用及机制的研究进展[D].石家庄:河北医科大学,2009.
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[35]Chuang KJ,Lee KY,Pan CH,et al.Effects of zinc oxide nanoparticles on human coronary artery endothelial cells[J].Food Chem Toxicol,2016,93:138-144.
[36]Yu X,Hong F,Zhang YQ.Cardiac inflammation involving in PKCεor ERK1/2-activated NF-kappa B signalling pathway in mice following exposure to titanium dioxide nanoparticles[J].Hazard Mater,2016,313:68-77.
[37]Luyts K,Smulders S,Napierska D,et al.Pulmonary and hemostatic toxicity of multi-walled carbon nanotubes and zinc oxide nanoparticles after pulmonary exposure in Bmal1 knockout mice[J].Part Fibre Toxicol,2014,11:61.
[38]Lane KJ,Levy JI,Scammell MK,et al.Association of modeled longterm personal exposure to ultrafine particles with inflammatory and coagulation biomarkers[J].Environ Int,2016,92-93:173-182.
[39]Chen T,Hu J,Chen C,et al.Cardiovascular effects of pulmonary exposure to titanium dioxide nanoparticles in Apo E knockout mice[J].Nanosci Nanotechnol,2013,13:3214-22.
[40]Stenmark KR,Davie N,Frid M,et al.Role of the adventitia in pulmonary vascular remodeling[J].Physiology(Bethesda),2006,21:134-45.
[41]Siddiqui MR,Komarova YA,Vogel SM,et al.Caveolin-1-e NOS signaling promotes p190Rho GAP:a nitration and endothelial permeability[J].Cell Biol,2011,193:841-850.
[42]Duran WN,Beuve AV,Sanchez FA.Nitric oxide,S-nitrosation,and endothelial permeability[J].IUBMB Life,2013,65:819-826.
[43]马语曼,孙琪,董玉,等.硝化应激参与衰老血管内皮功能障碍[J].首都医科大学学报,2015,36:908-914.
[44]王书美,李秋月,李康,等.采暖期不同阶段大气超细颗粒物污染特征初步研究[J].环境与健康杂志,2017,34(12):1039-1043.
[2]Chen R,Hu B,Liu Y,et al.Beyond PM2.5:The role of ultrafine particles on adverse health effects of air pollution[J].Biochim Biophys Acta,2016,1860:2844-2855.
[3]Li N,Georas S,Alexis N.A work group report on ultrafine particles(American Academy of Allergy,Asthma&Immunology):why ambient ultrafine and engineered nanoparticles should receive special attention for possible adverse health outcomes in human subjects[J].Allergy Clin Immunol,2016,138:386-396.
[4]Shrey K,Suchit A,Deepika D,et al.Air pollutants:the key stages in the pathway towards the development of cardiovascular disorders[J].Environ Toxicol Pharmacol,2011,31:1-9.
[5]Franchini M,Mannucci PM.Air pollution and cardiovascular disease[J].Thromb Res,2012,129:230-234.
[6]Lu F,Xu D,Cheng Y.Systematic review and meta-analysis of the adverse health effects of ambient PM2.5and PM10pollution in the Chinese population[J].Environ Res,2015,136:196-204.
[7]Morawska L,Control of particles indoor-state of the art[C]//Proceeding of Heathy Buidings,Espoo,Finland,2000.
[8]Metzger KB,Tolbert PE,Klein M,et a1.Ambient air pollution and cardiovascular emergency department visits[J].Epidemiology,2004,15:46-56.
[9]Lanki T,Pekkanen J,Aalto P,et a1.Associations of traffic related air pollutants with hospitalisation for first acute myoeardial in farction:the HEAPSS study[J].Occup Environ,2006,63:844-851.
[10]Von Klot S,Peters A,Aalto P,et al.Ambient air pollution is associated with increased risk of hospital cardiac readmissions of myocardial infaretion survivors in five European cities[J].Circulation,2005,112:3073-3079.
[11]Belleudi V,Faustini A,Stafoggia M,et a1.Impact of fine and ultrafine particles on emergency hospital admissions for cardiac and respiratory diseases[J].Epidemiology,2010,21:414-423.
[12]Forastiere F,Stafoggia M,Pieeiotto S,et al.A case-crossover analysis of out-of-hospital coronary deaths and air pollution in Rome,Italy[J].Am J Resp Crit Care Med,2005,12:1549-1555.
[13]Stlzel M,Breitner S,Cyrys J,et a1.Daily mortality and particulate matter in different size classes in Erfurt,Germany[J].Expo Sci Environ Epidemiol,2006,17:458-467.
[14]Dostál M,PastorkováA,Lanzinqer S,et al.Health effects of ambient ultrafine particles-the project UFIREG[J].Cas Lek Cesk,2015,154:176-180.
[15]Liu L,Breitner S,Schneider A,et al.Size-fractioned particulate air pollution and cardiovascular emergency room visits in Beijing,China[J].Environ Res,2013,121:52-63.
[16]Kooter IM,Boere AJF,Fokkens PH,et al.Response of spontaneously hypertensive rats to inhalation of fine and ultrafine particles from traffic:experimental controlled study[J].Part Fibre Toxicol,2006,3:7.
[17]Wottrich R,DiabatéS,Krug HF.Biological effects of ultrafine model particles in human macrophages and epithelial cells in mono-and co-culture[J].Int J Hyg Environ Health,2004,207:353-361.
[18]Nemmar A,Vanbilloen H,Hoylaerts MF,et a1.Passage of intratracheally instilled ultrafine particles from the lung into the systemic circulation in hamster[J].Am J Respir Crit Care Med,2001,164:1665-1668.
[19]Furuyama A,Kanno S,Kobayashi T,et a1.Extrapulmonary translocation of intratracheally instilled fine an d ultrafine particles via direct and alveolar macrophage associated routes[J].Arch Toxico1,2009,83:429-437.
[20]Br覿uner EV,Forchhammer L,M覬ller P,et al.Exposure to ultrafine particles from ambient air and oxidative stress-induced DNA damage[J].Environ Health Perspect,2007,115:1177-1182.
[21]Hertel S,Viehmann A,Moebus S,et al.Influence of short-term exposure to ultrafine and fine particles on systemic inflammation[J].Eur J Epidemiol,2010,25:581-592.
[22]Rtickerl R,Phipps RP,Schneider A,et al.Ultrafine particles and platelet activation in patients with coronary heart disease results from a prospective panel study[J].Part Fibre Toxicol,2007,4:1.
[23]Devlin RB,Smith CB,Schmitt MT,et al.Controlled exposure of humans with metabolic syndrome to concentrated ultrafine ambient particulate matter causes cardiovascular effects[J].Toxicol Sci,2014,140:61-72.
[24]Lin ZQ,Xi ZG,Chao FH,et al.Oxidative damage on lung tissue and peripheral blood in introtracheally treated rat by fine particulates in the city atmosphere[J].Biomed Environ Sci,2009,7:223-228.
[25]Lin ZQ,Liu LH,Xi ZG,et al.Single-walled carbon nanotubes promote rat vascular adventitial fibroblasts to transform into myofibroblasts by SM22-αexpression[J].Int J Nanomed,2012,7:4199-4206.
[26]Cheng WW,Lin ZQ,Ceng Q,et al.Single-wall carbon nanotubes induce oxidative stress in rat aortic endothelial cells[J].Toxicol Mech Meth,2012,22:286-276.
[27]Lin ZQ,Zhang HS,Huang JH,et al.Biodistribution of single-walled carbon nanotubes in rats[J].Toxicol Res,2014,3:497-502.
[28]王媛媛.硝化应激在心血管疾病中作用及机制的研究进展[D].石家庄:河北医科大学,2009.
[29]Gradinaru D,Borsa C,Ionescu C,et al.Oxidized LDL and NO synthesis:biomarkers of endothelial dysfunction and ageing[J].Mech Ageing Dev,2015,151:101-113.
[30]Zieske AW.Elevated serum C-reactive protein levels and advanced atherosclerosis in youth[J].Arterioscler Thromb Vasc Biol,2005,25:1237-1243.
[31]Rubbo H,Odonnell V,Nitric oxide,peroxynitrite and lipoxygenase in atherogenesis:mechanistic insights[J].Toxicology,2005,208:305-317.
[32]Leopold JA,Loscalzo J.Oxidative risk for atherothrombotic cardiovascular disease[J].Free Radic Biol Med,2009,47:1673-1706.
[33]Suhaimi NF,Jalaludin J.Biomarker as a research tool in linking exposure to air particles and respiratory health[J].Biomed Res Int,2015,DOI:10.1155/2015/962853.
[34]Du Y,Navab M,Shen M.Ambient ultrafine particles reduce endothelial nitric oxide production via S-glutathionylation of e NOS[J].Biochem Biophys Res Commun,2013,436:462-466.
[35]Chuang KJ,Lee KY,Pan CH,et al.Effects of zinc oxide nanoparticles on human coronary artery endothelial cells[J].Food Chem Toxicol,2016,93:138-144.
[36]Yu X,Hong F,Zhang YQ.Cardiac inflammation involving in PKCεor ERK1/2-activated NF-kappa B signalling pathway in mice following exposure to titanium dioxide nanoparticles[J].Hazard Mater,2016,313:68-77.
[37]Luyts K,Smulders S,Napierska D,et al.Pulmonary and hemostatic toxicity of multi-walled carbon nanotubes and zinc oxide nanoparticles after pulmonary exposure in Bmal1 knockout mice[J].Part Fibre Toxicol,2014,11:61.
[38]Lane KJ,Levy JI,Scammell MK,et al.Association of modeled longterm personal exposure to ultrafine particles with inflammatory and coagulation biomarkers[J].Environ Int,2016,92-93:173-182.
[39]Chen T,Hu J,Chen C,et al.Cardiovascular effects of pulmonary exposure to titanium dioxide nanoparticles in Apo E knockout mice[J].Nanosci Nanotechnol,2013,13:3214-22.
[40]Stenmark KR,Davie N,Frid M,et al.Role of the adventitia in pulmonary vascular remodeling[J].Physiology(Bethesda),2006,21:134-45.
[41]Siddiqui MR,Komarova YA,Vogel SM,et al.Caveolin-1-e NOS signaling promotes p190Rho GAP:a nitration and endothelial permeability[J].Cell Biol,2011,193:841-850.
[42]Duran WN,Beuve AV,Sanchez FA.Nitric oxide,S-nitrosation,and endothelial permeability[J].IUBMB Life,2013,65:819-826.
[43]马语曼,孙琪,董玉,等.硝化应激参与衰老血管内皮功能障碍[J].首都医科大学学报,2015,36:908-914.
[44]王书美,李秋月,李康,等.采暖期不同阶段大气超细颗粒物污染特征初步研究[J].环境与健康杂志,2017,34(12):1039-1043.