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首页> 外文期刊>Environmental Science and Pollution Research >Associations of soluble metals and lung and liver toxicity in mice induced by fine particulate matter originating from a petrochemical complex
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Associations of soluble metals and lung and liver toxicity in mice induced by fine particulate matter originating from a petrochemical complex

机译:源自石油化学复合物的细颗粒物质诱导的小鼠中可溶性金属和肺和肝毒性的关联

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摘要

Adverse health effects have been observed in nearby residents due to exposure to petrochemical-derived chemicals. The objective of this study was to examine associations of soluble metals with lung and liver toxicity in fine particulate matter (PM2.5) in the vicinity of a petrochemical complex. PM(2.5)was collected in the vicinity of a petrochemical complex of Mailiao Township (Yunlin County, Taiwan) to investigate lung and liver toxicity in BALB/c mice. The PM(2.5)concentration was 30.2 +/- 11.2 mu g/m(3), and the PM(2.5)was clustered in major local emissions (19.1 mu g/m(3)) and minor local emissions (14.1 mu g/m(3)) using a k-means clustering model. The PM2.5(50 and 150 mu g/kg) and PM2.5-equivalent soluble nickel (Ni), vanadium (V), and lead (Pb) concentrations were intratracheally instilled into BALB/c mice. PM(2.5)and V significantly decreased the tidal volume after exposure (p < 0.05). The peak expiratory flow (PEF) and peak inspiratory flow (PIF)/PEF ratio were significantly altered by 150 mu g/kg V (p < 0.05). V and Pb significantly increased total protein and lactate dehydrogenase (LDH) levels in bronchoalveolar lavage fluid (BALF) (p < 0.05). Interleukin (IL)-6 in BALF significantly increased after exposure to Pb (p < 0.05) accompanied by lung inflammatory infiltration. PM(2.5)and Pb significantly increased levels of 8-isoprostane (p < 0.05). The level of caspase-3 activity significantly increased after exposure to Pb (p < 0.05). LDH in the liver was significantly increased by PM2.5(p < 0.05). 8-Isoprostane in the liver was significantly increased by PM(2.5)and Pb (p < 0.05). IL-6 in the liver was significantly increased by PM2.5, Ni, V, and Pb after exposure (p < 0.05), accompanied by liver inflammatory infiltration. Our results demonstrated that V in PM(2.5)was associated with an increase in 8-isoprostane for all emissions and major local petrochemical emissions. In conclusion, V contributes to in vivo liver toxicity induced by PM(2.5)in the vicinity of a petrochemical complex.
机译:由于暴露于石化化学品,附近居民已经观察到不良健康效果。本研究的目的是研究可溶性金属与肺和肝毒性在石油化学复合物附近的细颗粒物质(PM2.5)中的缔合品。 PM(2.5)收集在Mailioo乡(台湾云林县)的石油化工复合物附近,探讨Balb / C小鼠的肺和肝毒性。 PM(2.5)浓度为30.2 +/-11.2μmg/ m(3),PM(2.5)聚集在主要局部排放(19.1μg/ m(3))和轻微的局部排放(14.1μg / m(3))使用k-means聚类模型。 PM2.5(50μmg/ kg)和pm2.5-当量可溶性镍(Ni),钒(V)和铅(Pb)浓度脑内滴入Balb / c小鼠。 PM(2.5)和V暴露后显着降低潮气量(P <0.05)。峰值呼气流(PEF)和峰值吸气流动(PIF)/ PEF比率明显改变150μmg/ kg v(p <0.05)。 V和PB在支气管肺泡灌洗液(BALF)中显着增加了总蛋白质和乳酸脱氢酶(LDH)水平(P <0.05)。在暴露于Pb(P <0.05)后,BALF的白细胞介素(IL)-6显着增加(P <0.05)伴随着肺炎炎症浸润。 PM(2.5)和PB显着增加8-异前烷水平(P <0.05)。在暴露于Pb后,Caspase-3活性的水平显着增加(P <0.05)。 PM2.5的LDH显着增加(P <0.05)。 PM(2.5)和Pb(P <0.05)显着增加肝脏中的8-异戊二醇烷。在暴露(P <0.05)后PM2.5,Ni,V和PB,肝脏中的IL-6显着增加(P <0.05),伴有肝脏炎症浸润。我们的结果表明,PM(2.5)的v与所有排放和主要局部石化排放量增加了8-异前烷。总之,v有助于PM(2.5)在石油化学复合物附近诱导的体内肝脏毒性。

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