本文選題：氡 + 亞砷酸鈉　； 參考：《蘇州大學(xué)》2013年碩士論文

【摘要】：目的探討氡與亞砷酸鈉染毒永生化人上皮細(xì)胞（HBE cells）聯(lián)合作用類型及聯(lián)合染毒對(duì)HBE細(xì)胞氧化損傷和DNA損傷的影響。 方法（1）以HBE細(xì)胞為研究對(duì)象，將HBE細(xì)胞單獨(dú)暴露于20000Bq/m3的氡染毒不同時(shí)間（0～75min）、不同劑量（0～50000μmol/L）的亞砷酸鈉以及二者的聯(lián)合染毒，采用活細(xì)胞計(jì)數(shù)試劑盒(CCK-8)檢測(cè)細(xì)胞存活率。通過中效原理計(jì)算不同時(shí)間氡暴露和不同劑量亞砷酸鈉染毒聯(lián)合作用的聯(lián)合指數(shù)（combinationindex，CI）。（2）以不同時(shí)間氡暴露（20000Bq/m3，10、20和40min）和不同濃度亞砷酸鈉（1.5、3.0和6.0μmol/L）處理HBE細(xì)胞，測(cè)定氡、亞砷酸鈉單獨(dú)及聯(lián)合染毒后， HBE細(xì)胞活性氧（reactive oxygen species， ROS）、丙二醛（malondialdehyde，MDA）含量和超氧化物歧化酶（superoxi dismutase，SOD）活力的變化；通過彗星實(shí)驗(yàn)檢測(cè)氡、亞砷酸鈉單獨(dú)及聯(lián)合染毒后HBE細(xì)胞的DNA損傷情況；（3）通過Western blot檢測(cè)在氡、亞砷酸鈉單獨(dú)及聯(lián)合染毒后24小時(shí)，DNA損傷蛋白γH2AX和DNA修復(fù)蛋白R(shí)ad51。 結(jié)果（1）氡與亞砷酸鈉單獨(dú)或聯(lián)合染毒對(duì)HBE細(xì)胞均有抑制作用；不同時(shí)間氡暴露和不同劑量亞砷酸鈉聯(lián)合染毒的聯(lián)合指數(shù)CI1，，表明二者呈現(xiàn)協(xié)同作用。（2）在單獨(dú)染毒的條件下，與空白對(duì)照組相比，氡單獨(dú)染毒組和亞砷酸鈉單獨(dú)染毒組ROS和MDA含量均隨暴露時(shí)間延長(zhǎng)和濃度增大顯著升高，SOD活力均顯著下降（P0.05）；且分別隨著氡暴露時(shí)間的延長(zhǎng)和亞砷酸鈉染毒劑量的增加，HBE細(xì)胞內(nèi)MDA和ROS含量均呈現(xiàn)明顯的上升趨勢(shì)，而SOD活力明顯下降。當(dāng)聯(lián)合染毒時(shí)，分別在氡暴露時(shí)間恒定以及亞砷酸鈉劑量恒定的條件下，各聯(lián)合染毒組HBE細(xì)胞ROS和MDA的含量均明顯增加（P0.05）；SOD活力均顯著下降（P0.05）。（3）彗星實(shí)驗(yàn)：與對(duì)照組相比，氡單獨(dú)染毒組及亞砷酸鈉單獨(dú)染毒組，各組HBE細(xì)胞的尾部DNA百分含量、尾距和Olive尾距均顯著增加（P0.05）；當(dāng)聯(lián)合染毒時(shí)，在氡暴露時(shí)間恒定以及亞砷酸鈉劑量恒定的條件下，聯(lián)合染毒組HBE細(xì)胞尾部DNA百分含量、尾距和Olive尾距均顯著增加，且均高于對(duì)照組、氡單獨(dú)染毒組及亞砷酸鈉單獨(dú)染毒組（P0.05）。（4）Western blot實(shí)驗(yàn)：與對(duì)照組比較，各染毒組的DNA損傷蛋白γH2AX表達(dá)量明顯增加，而DNA修復(fù)蛋白R(shí)ad51表達(dá)量下降；與氡單獨(dú)染毒組和亞砷酸鈉單獨(dú)染毒組相比，聯(lián)合染毒組γH2AX表達(dá)量明顯增加，Rad51表達(dá)量明顯降低，且隨著染亞砷酸鈉劑量的增加，γH2AX表達(dá)量呈現(xiàn)上升趨勢(shì)，Rad51表達(dá)量呈現(xiàn)下降趨勢(shì)。 結(jié)論 1、氡與亞砷酸鈉聯(lián)合染毒HBE細(xì)胞具有協(xié)同抑制細(xì)胞生長(zhǎng)的作用。 2、氡與亞砷酸鈉聯(lián)合染毒HBE細(xì)胞，通過造成嚴(yán)重的氧化損傷和DNA損傷，抑制其生長(zhǎng)。
[Abstract]:Objective to investigate the combined effects of radon and sodium arsenite exposure on immortalized human epithelial cells (HBE cells) and the effects of combined exposure on oxidative damage and DNA damage of HBE cells. Methods (1) HBE cells were exposed to 20 000 Bq / m 3 radon for different time (0~75min), different doses (0 ~ 50000 渭 mol / L) of sodium arsenite and combined exposure. The survival rate of HBE cells was measured by living cell count kit (CCK-8). The combined index CI). (2 of radon exposure at different time and different doses of sodium arsenite was calculated by medium effect principle. HBE cells were treated with different time radon exposure (20000Bq / m31020 and 40min) and different concentrations of sodium arsenite (1.53.0 渭 mol / L and 6.0 渭 mol / L). The contents of reactive oxygen species (Ros), malondialdehyde (malondialdehyde) and the activity of superoxi dismutase (superoxi dismutase) in HBE cells were detected by comet assay. (3) the DNA damage protein 緯 H 2AX and DNA repair protein Rad51 were detected 24 hours after radon and sodium arsenite exposure alone or in combination by Western blot. Results (1) Radon and sodium arsenite alone or in combination had inhibitory effects on HBE cells, the combined index CI1 of radon exposure at different time and sodium arsenite at different doses showed synergistic effect. (2) under the condition of single exposure to radon and sodium arsenite, Compared with the blank control group, Ros and MDA contents in radon alone and sodium arsenite groups decreased significantly with the prolongation of exposure time and the increase of concentration (P0.05). With the prolongation of radon exposure time and the increase of sodium arsenite exposure, the contents of MDA and Ros in HBE cells showed an obvious upward trend, while the activity of SOD decreased significantly. Under the condition of constant radon exposure time and constant dose of sodium arsenite, the contents of Ros and MDA in HBE cells of each combined exposure group were significantly increased (P0.05), and the activity of). (was significantly decreased (P0.05) Comet assay: compared with the control group, the Ros and MDA contents of HBE cells in each combined exposure group were significantly higher than those in the control group. The tail DNA content, tail distance and Olive tail distance of HBE cells in each group were significantly increased in radon alone and sodium arsenite groups (P0.05), and under the condition of constant radon exposure time and constant dose of sodium arsenite, The percentage of tail DNA, tail distance and Olive tail distance of HBE cells in combined exposure group were significantly higher than those in control group. Western blot test of radon alone and sodium arsenite exposure group (P0.05). (4): compared with control group. The expression of DNA damage protein 緯 H 2AX increased significantly, but the expression of DNA repair protein Rad51 decreased, compared with radon alone and sodium arsenite alone, the expression of 緯 H 2AX in combined exposure group was significantly higher than that in sodium arsenite group, and the expression of 緯 H 2AX in combined exposure group was significantly lower than that in radon alone group and sodium arsenite group. With the increase of sodium arsenite, the expression of 緯 H 2AX increased and Rad51 decreased. Conclusion 1. HBE cells exposed to radon and sodium arsenite have synergistic effects on cell growth. 2. HBE cells exposed to radon and sodium arsenite combined with sodium arsenite can inhibit the growth of HBE cells by causing severe oxidative damage and DNA damage.
【學(xué)位授予單位】：蘇州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2013
【分類號(hào)】：R114

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本文編號(hào)：2050386