北方某燃煤区PM_(2.5)对秀丽隐杆线虫毒效应的初步研究
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摘要
目的探索北方某燃煤地区室外大气细颗粒物(PM_(2.5))水溶性离子对模式生物秀丽隐杆线虫的急性致死效应,并探究其对线虫生长发育、神经行为和衰老进程的影响。方法以空气质量等级为优、轻度、中度和重度污染时采集的燃煤地区PM_(2.5)水溶液样本(浓度当量分别为17.5、101.4、130.7和188.9μg/ml,对应于优、轻、中和重组)对同步化的L1和L4期线虫分别进行染毒,测定其存活率、体长、体宽、咽泵振动频率、肠道自发荧光和热耐受力变化。结果 L1期线虫染毒72 h后,优组、轻组和中组的体长均有改变(P<0.05),重组的体宽差异有统计学意义(P<0.01),轻、中和重组的自发荧光强度均比对照组明显增强(P<0.01);L4期线虫染毒24 h,中度和重度污染组体长体宽、咽泵频率的改变与对照组比较,差异有统计学意义(P<0.01),重度污染组肠道自发荧光比对照组明显增强(P<0.01),继续染毒至72 h时优组和重组肠道荧光明显增强(P<0.01),染毒至第5天时各染毒组在热应激条件下平均寿命明显缩短(P<0.05),染毒至10天时轻度和重度污染组热耐受力比对照组明显减弱,差异有统计学意义(P<0.01)。结论燃煤区来源的PM_(2.5)可对线虫生长发育、神经运动等产生毒性效应,并加速线虫的衰老进程,提示有必要进一步开展其毒性分子机制研究。
Objective To study the toxic effects of water-soluble PM_(2.5) exposure on survival, growth and development,neuron function and aging on C. elegans, and evaluate the toxicity of the water-soluble components of outdoor PM_(2.5) samples from a coal-fired region in northern China. Methods Nematodes at L1 stage or L4 stage were exposed to PM_(2.5)(group-E, group-L, group-M, group-H, with concentration of 17.5, 101.4, 130.7 and 188.9 μg/ml respectively), the survival rate, body length and width, pharyngeal pump vibration frequency were recorded, and the level of intestinal autofluorescence as well as heat tolerance were measured. Result PM_(2.5) didn't induce acute lethal toxicity to C. elegans. For L1 stage nematodes,the body length of group-E, group-L and group-M were statistically different with that from control group(P<0.05), and the body width of group-H was statistically significant(P<0.01). The intestinal fluorescence of group-L, group-M and group-H were significantly higher than that of the control group(P<0.01). For nematodes at L4 stage, the body size and pharyngeal pump frequency of group-M and group-H were statistically different from the control group;At 24 h the intestinal autofluorescence in group-H increased significantly(P<0.01), and the fluorescence of group-E and group-H were significantly increased when the exposure was continued for 72 hours(P<0.01). The average lifespan of the exposed groups was significantly shortened under heat stress on day 5(P<0.05), and the heat tolerance of group-L and group-H were significantly weaker than that of the control group on day 10(P<0.01). Conclusion PM_(2.5) from coal combustion could induce toxic effects on nematode growth and nerve function, furthermore, accelerate the aging process of nematodes,which suggesting that further study on its molecular mechanism is necessary.
Objective To study the toxic effects of water-soluble PM_(2.5) exposure on survival, growth and development,neuron function and aging on C. elegans, and evaluate the toxicity of the water-soluble components of outdoor PM_(2.5) samples from a coal-fired region in northern China. Methods Nematodes at L1 stage or L4 stage were exposed to PM_(2.5)(group-E, group-L, group-M, group-H, with concentration of 17.5, 101.4, 130.7 and 188.9 μg/ml respectively), the survival rate, body length and width, pharyngeal pump vibration frequency were recorded, and the level of intestinal autofluorescence as well as heat tolerance were measured. Result PM_(2.5) didn't induce acute lethal toxicity to C. elegans. For L1 stage nematodes,the body length of group-E, group-L and group-M were statistically different with that from control group(P<0.05), and the body width of group-H was statistically significant(P<0.01). The intestinal fluorescence of group-L, group-M and group-H were significantly higher than that of the control group(P<0.01). For nematodes at L4 stage, the body size and pharyngeal pump frequency of group-M and group-H were statistically different from the control group;At 24 h the intestinal autofluorescence in group-H increased significantly(P<0.01), and the fluorescence of group-E and group-H were significantly increased when the exposure was continued for 72 hours(P<0.01). The average lifespan of the exposed groups was significantly shortened under heat stress on day 5(P<0.05), and the heat tolerance of group-L and group-H were significantly weaker than that of the control group on day 10(P<0.01). Conclusion PM_(2.5) from coal combustion could induce toxic effects on nematode growth and nerve function, furthermore, accelerate the aging process of nematodes,which suggesting that further study on its molecular mechanism is necessary.
引文
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[22] Shen L,Hu Y,Cai T,et al.Regulation of longevity by genes required for the functions of AIY interneuron in nematode Caenorhabditis elegans[J].Mech Ageing Dev,2010,131(11):732-738.
[23] Houthoofd K,Braeckman BP,Johnson TE,et al.Life extension via dietary restriction is independent of the Ins/IGF-1 signalling pathway in Caenorhabditis elegans[J].Exp Gerontol,2003,38(9):947-954.
[24] Libina N,Berman JR,Kenyon C.Tissue-Specific Activities of C.elegans DAF-16 in the Regulation of Lifespan[J].Cell,2003,115(4):489-502.
[25] Lithgow GJ,Walker GA.Stress resistance as a determinate of C.elegans lifespan [J].Mech Ageing Dev,2002,123(7):765-771.
[2] Lelieveld J,Evans JS,Fnais M,et al.The contribution of outdoor air pollution sources to premature mortality on a global scale[J].Nature,2015,525 (7569):367-371.
[3] Lim SS,Vos T,Flaxman AD,et al.A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions,1990-2010:a systematic analysis for the Global Burden of Disease Study [J].Lancet,2012,380(9859):2197-2223.
[4] 曾强,李国星,张磊,等.大气污染对健康影响的疾病负担研究进展[J].环境与健康杂志,2015,32(1):85-90.
[5] Dominici F,Wang Y,Correia AW,et al.Chemical composition of fine particulate matter and life expectancy:In 95 US counties between 2002 and 2007[J].Epidemiology,2015,26(4):556-564.
[6] Ballester F,Tenías JM,Pérez-Hoyos S.Air pollution and emergency hospital admissions for cardiovascular diseases in Valencia Spain[J].J Epidemiol Community Health,2001,55(1):57-65.
[7] Zhang X,Duan H,Gao F,et al.Increased micronucleus,nucleoplasmic bridge,and nuclear bud frequencies in the peripheral blood lymphocytes of diesel engine exhaust-exposed workers[J].Toxicol Sci,2015,143(2):408-417.
[8] Zhang R,Dai Y,Zhang X,et al.Reduced pulmonary function and increased pro-inflammatory cytokines in nanoscale carbon black-exposed workers[J].Part Fibre Toxicol,2014,11:73.
[9] EPA.Air Quality Criteria for Particulate Matter (Final Report,2004)[EB/OL].(2014-03-12).https://cfpub.epa.gov/ncea/risk/recordisplay.cfm?deid=87903.
[10] P.Pokorná,Hovorka J,M.Klán,et al.Source apportionment of size resolved particulate matter at a European air pollution hot spot[J].Sci Total Environ,2015,502:172-183.
[11] Li Y,Gao S,Jing H,et al.Correlation of chemical acute toxicity between the nematode and the rodent[J].Toxicol Res,2013,2(6):403-412.
[12] 王云彪,侯晓丽,武海涛,等.PM2.5对秀丽隐杆线虫的毒性效应[J].城市环境与城市生态杂志,2012,25(6):10-13.
[13] Sun L,Wu Q,Liao K,et al.Contribution of heavy metals to toxicity of coal combustion related fine particulate matter (PM2.5) in Caenorhabditis elegans:with wild-type or susceptible genetic background[J].Chemosphere,2016,144:2392-2400.
[14] 马彦,魏建荣,陶晶,等.北京市2013年冬季极端天气时室内细颗粒物浓度水平及其特征研究[J].中华预防医学杂志,2013,47(9):832-836.
[15] Gao S,Chen W,Zeng Y,et al.Classification and prediction of toxicity of chemicals using an automated phenotypic profiling of Caenorhabditis elegans[J].Pharm & Toxicol,(2018)19:18.https://doi.org/10.1186/s40360-018-0208-3.
[16] 孔玲,李子南,张楠,等.PM2.5对线虫热耐受性的影响及线虫喂饲菌灭活方法探索[J].毒理学杂志,2017,31(3):165-171.
[17] 王心宇,田佩瑶,陶晶,等.室内外PM2.5中主要水溶性离子分布水平及特征研究[J].首都公共卫生,2017,(5):7-11.
[18] Zhao Y,Lin Z,Jia R,et al.Transgenerational effects of traffic-related fine particulate matter (PM2.5) on nematode Caenorhabditis elegans[J].J Hazard Mater,2014(274):106-114.
[19] Ziyue Chen,Jun Cai,Bingbo Gao,et al.Detecting the causality influence of individual meteorological factors on local PM2.5 concentration in the Jing-Jin-Ji region[J].Sci Rep,2017,7:40735.
[20] James PM,David MR,Alexander G,et al.Eat-2 and eat-18 are required for nicotinic neurotransmission in the Caenorhabditis elegans pharynx[J].Genetics,2004,166(1):161-169.
[21] 田雨.久效磷对秀丽隐杆线虫(Caenorhabditis elegans)多种毒性效应的当量评价[D].青岛:中国海洋大学,2011.
[22] Shen L,Hu Y,Cai T,et al.Regulation of longevity by genes required for the functions of AIY interneuron in nematode Caenorhabditis elegans[J].Mech Ageing Dev,2010,131(11):732-738.
[23] Houthoofd K,Braeckman BP,Johnson TE,et al.Life extension via dietary restriction is independent of the Ins/IGF-1 signalling pathway in Caenorhabditis elegans[J].Exp Gerontol,2003,38(9):947-954.
[24] Libina N,Berman JR,Kenyon C.Tissue-Specific Activities of C.elegans DAF-16 in the Regulation of Lifespan[J].Cell,2003,115(4):489-502.
[25] Lithgow GJ,Walker GA.Stress resistance as a determinate of C.elegans lifespan [J].Mech Ageing Dev,2002,123(7):765-771.
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