纳米黑碳与砷的联合细胞毒性及遗传毒性研究

发布时间：2018-04-12 01:00

本文选题：纳米黑碳 + 砷　；参考：《中国科学技术大学》2017年硕士论文

【摘要】：大气颗粒污染物化学组成成分复杂,含碳颗粒物占PM25(细颗粒)重量的40%-60%,占PM10(可吸入颗粒)重量的25%-35%。目前,黑碳作为城市大气环境污染物的重要组成成分已经被世界癌症研究组织(IARC)归类为2B类致癌物,与心血管、呼吸系统的疾病发生都有关系,并且对神经系统和生殖系统也有不利影响。黑碳颗粒粒径较小,比表面积较大,可吸附其他重金属元素及微量元素,是众多有机污染物和重金属的重要载体。砷(As),作为大气污染物的重要组成部分,已被美国环境保护局(USEPA)和IARC列为环境致癌物。然而,黑碳与砷联合毒性效应的研究还鲜有报道。本论文一方面通过对纳米黑碳本身的生物毒性进行研究,发现纳米黑碳具有一定的细胞毒性,可诱导细胞活力下降,促使细胞内源性凋亡密切相关的信号转导通路关键蛋白Caspase 3/7蛋白活化表达量增高;且实验结果表明细胞内ROS水平的升高可能是纳米黑碳诱导毒性效应的机制之一。另一方面,我们以人鼠杂交瘤细胞(AL细胞)这一体外哺乳动物细胞的基因突变检测系统为基础,对纳米黑碳和重金属砷的联合毒性进行研究发现,纳米黑碳和砷可联合诱导AL细胞存活率显著下降,CD59基因突变率显著上升,且这种毒性效应强于纳米黑碳和砷独自诱导。接着对于纳米黑碳和砷诱导联合毒性效应的机制进行研究,发现纳米黑碳和砷共处理也可诱导细胞内ROS水平浓度依赖式升高,且高于两者独自诱导,暗示我们ROS的上调在纳米黑碳和砷诱导联合毒性的过程中有重要作用。本论文为揭示黑碳和重金属污染物潜在的联合健康危害和风险提供一定的实验证据。
[Abstract]:The chemical composition of atmospheric particulate pollutants is complex. Carbon particles account for 40-60% of PM25 (fine particles) and 25-35% of PM10 (inhalable particles).At present, black carbon, as an important component of urban atmospheric environmental pollutants, has been classified as 2B carcinogen by the World Cancer Research Organization (IARC), which is related to cardiovascular and respiratory diseases.It also has adverse effects on the nervous system and the reproductive system.Black carbon particles with small particle size and large specific surface area can adsorb other heavy metal elements and trace elements and are important carriers of many organic pollutants and heavy metals.As an important component of atmospheric pollutants, arsenic aspartate has been listed as environmental carcinogen by USEPA and IARC.However, studies on the combined toxicity of black carbon and arsenic are rarely reported.On the one hand, by studying the biological toxicity of nano-black carbon, we found that nano-black carbon has certain cytotoxicity, which can induce the decline of cell viability.The activation and expression of the signal transduction pathway key protein Caspase 3 / 7, which is closely related to intracellular apoptosis, was increased, and the results indicated that the increase of ROS level might be one of the mechanisms of the toxicity induced by nano-black carbon.On the other hand, based on the human mouse hybridoma cell (AL cell), a gene mutation detection system of mammalian cells in vitro, we studied the joint toxicity of nano-black carbon and arsenic.The survival rate of AL cells induced by nano-black carbon and arsenic was significantly decreased, and the mutation rate of CD59 gene was significantly increased, and the toxicity was stronger than that induced by nano-black carbon and arsenic alone.Then the mechanism of co-treatment with nano-black carbon and arsenic was studied. It was found that co-treatment of nano-black carbon and arsenic could also induce the increase of intracellular ROS level in a concentration-dependent manner, and was higher than that induced by both alone.It is suggested that the upregulation of our ROS may play an important role in the process of co-toxicity induced by nano black carbon and arsenic.This paper provides some experimental evidence for revealing the potential joint health hazards and risks of black carbon and heavy metal pollutants.
【学位授予单位】：中国科学技术大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R994.6;X513

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