本文選題：納米黑碳 + 砷��； 參考：《中國科學(xué)技術(shù)大學(xué)》2017年碩士論文

【摘要】：大氣顆粒污染物化學(xué)組成成分復(fù)雜,含碳顆粒物占PM25(細(xì)顆粒)重量的40%-60%,占PM10(可吸入顆粒)重量的25%-35%。目前,黑碳作為城市大氣環(huán)境污染物的重要組成成分已經(jīng)被世界癌癥研究組織(IARC)歸類為2B類致癌物,與心血管、呼吸系統(tǒng)的疾病發(fā)生都有關(guān)系,并且對神經(jīng)系統(tǒng)和生殖系統(tǒng)也有不利影響。黑碳顆粒粒徑較小,比表面積較大,可吸附其他重金屬元素及微量元素,是眾多有機污染物和重金屬的重要載體。砷(As),作為大氣污染物的重要組成部分,已被美國環(huán)境保護(hù)局(USEPA)和IARC列為環(huán)境致癌物。然而,黑碳與砷聯(lián)合毒性效應(yīng)的研究還鮮有報道。本論文一方面通過對納米黑碳本身的生物毒性進(jìn)行研究,發(fā)現(xiàn)納米黑碳具有一定的細(xì)胞毒性,可誘導(dǎo)細(xì)胞活力下降,促使細(xì)胞內(nèi)源性凋亡密切相關(guān)的信號轉(zhuǎn)導(dǎo)通路關(guān)鍵蛋白Caspase 3/7蛋白活化表達(dá)量增高;且實驗結(jié)果表明細(xì)胞內(nèi)ROS水平的升高可能是納米黑碳誘導(dǎo)毒性效應(yīng)的機制之一。另一方面,我們以人鼠雜交瘤細(xì)胞(AL細(xì)胞)這一體外哺乳動物細(xì)胞的基因突變檢測系統(tǒng)為基礎(chǔ),對納米黑碳和重金屬砷的聯(lián)合毒性進(jìn)行研究發(fā)現(xiàn),納米黑碳和砷可聯(lián)合誘導(dǎo)AL細(xì)胞存活率顯著下降,CD59基因突變率顯著上升,且這種毒性效應(yīng)強于納米黑碳和砷獨自誘導(dǎo)。接著對于納米黑碳和砷誘導(dǎo)聯(lián)合毒性效應(yīng)的機制進(jìn)行研究,發(fā)現(xiàn)納米黑碳和砷共處理也可誘導(dǎo)細(xì)胞內(nèi)ROS水平濃度依賴式升高,且高于兩者獨自誘導(dǎo),暗示我們ROS的上調(diào)在納米黑碳和砷誘導(dǎo)聯(lián)合毒性的過程中有重要作用。本論文為揭示黑碳和重金屬污染物潛在的聯(lián)合健康危害和風(fēng)險提供一定的實驗證據(jù)。
[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.
【學(xué)位授予單位】：中國科學(xué)技術(shù)大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R994.6;X513

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