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研究生:吳奕瑩
研究生(外文):Yi-Ying Wu
論文名稱:中國倉鼠卵巢細胞受紫外線誘導及其被秋水仙素加成的細胞死亡的特性
論文名稱(外文):Characterization of UVC-induced cell death that is promoted by colcemid in CHO-K1 cells
指導教授:劉銀樟
指導教授(外文):Yin-Chang Liu
學位類別:碩士
校院名稱:國立清華大學
系所名稱:生命科學系
學門:生命科學學門
學類:生物學類
論文種類:學術論文
論文出版年:2002
畢業學年度:90
語文別:英文
論文頁數:62
中文關鍵詞:中國倉鼠卵巢細胞細胞自裁性死亡紫外線秋水仙素
外文關鍵詞:CHO.K1apoptosisUVCcolcemid
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哺乳動物細胞擁有顯著的功能去反應不同的壓迫,特別是會引響基因穩定性的那些壓迫。紫外線已知會產生光產物和嘧啶雙體,使細胞週期行進停止以修復DNA,或走向細胞自裁性死亡(apoptosis)。我們實驗室之前的研究發現中國倉鼠卵巢細胞(CHO.K1)的p21表現缺失,其照射紫外線(UVC)後產生大量的細胞死亡,並且若接受紫外線照射後存在於抗有絲分裂的藥物中,會形成加成性的細胞死亡。在此,我們描述了一些現象或機制以期進一步去明瞭此細胞死亡。紫外線所造成的中國倉鼠卵巢細胞死亡與秋水仙素(colcemid),一種抗有絲分裂的藥物,所加成的細胞死亡都是屬於細胞自裁性死亡。紫外線照射所產生的DNA傷害造成紫外線誘發的細胞自裁,而非活性態氧族(ROS)(Liao, 2001)及死亡受體的活化(death receptor activation)。雖然p21缺失,中國倉鼠卵巢細胞仍然表現正常的DNA修復能力。即使如此,p21的缺失及其失去抑制CDK的活性仍是中國倉鼠卵巢細胞受紫外線照射會大量死亡的原因。另外,秋水仙素加成紫外線所誘發的細胞死亡過程中並不會使粒線體的膜電位下降或是使鈣離子釋放至細胞質內。而Cdk1的過於活化與DNA修復的延遲也許才是造成秋水仙素加成紫外線誘發細胞自裁死亡的因素。

Mammalian cells possess a remarkable repertoire of responses to diverse stresses, particularly those inflicting genetic stability. UV, which is well known to generate photoproducts and the pyrimidine dimer may arrest cell cycle progression for DNA repair or lead to apoptosis by evoking checkpoint pathway. Previous researches in our laboratory has found that CHO.K1 cells, deficient in expression of p21 WAF1/CIP1, display UVC-induced cell death, which is promoted by the presence of anti-mitotic drugs in the cells following UVC irradiation. Here, we describe some phenomena or mechanisms to elucidate the cell death in advance. In CHO.K1 cells, UVC-induced cell death which is exacerbated in presence of colcemid (a mitotic inhibitor) belongs to apoptosis. UVC-induced DNA damage, neither ROS (Liao, 2001) nor death receptor activation, contributes to UVC-induced apoptosis. Although p21 WAF1/CIP1 is deficient in CHO.K1 cells, the cells exhibit normal nucleotide excision repair of UVC-induced DNA damage. However, the massive UVC-induced apoptosis in CHO.K1 cells is still due to the defect in p21waf1/cip1 so that CDK activity is not inhibited. During colcemid-promoted apoptosis following UVC irradiation, neither decrease of mitochondrial membrane potential nor release of Ca2+ in cytosol is observed. Over-activation of cdk1 and delay of DNA repair may result in the promoted apoptosis by colcemid.

Ⅰ. Table of Content …………………………………………………… 1
Ⅱ. Acknowledgements ………………………………………………………… 2
Ⅲ. English abstract ……………………………………………………………. 3
Ⅳ. Chinese abstract ……………………………………………………………. 4
Ⅴ. Introduction ………………………………………………………………… 5
Ⅵ. Materials & Methods ………………………………………………………. 9
Ⅶ. Results ……………………………………………………………………… 19
Ⅷ. Discussion ………………………………………………………………….. 30
Ⅸ. References ………………………………………………………………….. 33
Ⅹ. Tables & Figures ……………………………………………………………. 37

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