English  |  正體中文  |  简体中文  |  Items with full text/Total items : 43312/67235
Visitors : 2107242      Online Users : 10
RC Version 5.0 © Powered By DSPACE, MIT. Enhanced by NTU/NCHU Library IR team.
National Chung Hsing University Institutional Repository - NCHUIR > 中興大學 > 校內出版品 > 工學院 > 期刊-興大工程學刊(原興大工程學報) > 第13卷 第3期 >  4-鄰位醌類衍生物誘發小牛胸腺DNA去鹼基核酸及單鏈斷裂生成之研究

Please use this identifier to cite or link to this item: http://nchuir.lib.nchu.edu.tw/handle/309270000/142538

標題: 4-鄰位醌類衍生物誘發小牛胸腺DNA去鹼基核酸及單鏈斷裂生成之研究
作者: 林伯雄;廖宏慈;侯國隆
Contributors: 工學院
關鍵字: 去鹼基核酸;DNA單股斷鏈;氧化DNA損害
日期: 2002-11
Issue Date: 2013-05-02 21:14:57 (UTC+8)
Publisher: 國立中興大學工學院;Airiti Press Inc.
摘要: 本研究之主知即在於應用生物性指標(biomarker)探討氯酚之鄰位?類化物,4-單氯烴?(4-chlorocatechol, 4-ClCAT)能否經由不斷氧化還原循環(redox cycle)進而生成活潑性氧(reactive oxygen species, ROS)對DNA造成破壞作用,包括去鹼基核酸(paurinic/apyridiminic, AP sites)及DNA單鏈斷裂(single strand break, SSB)進行測試。研究結果顯示,4-ClCAT於過渡性金屬銅Cu(II)存在之環境下能對小牛胸腺DNA同時誘發DNA SSB及AP sites之核酸損害作用。ROS移除劑,例如氫氧自由基移除劑DMSO(6%)、甲醇(6%),超氧自由基移除劑superoxide dismatase (SOD)對DNA SSB及AP sites,均無抑制作用,但過氧化氫酵素(catalase)具有抑制效應,顯示其中實際參與核酸損害作用之ROS分子為H2O2。同時,Cu(I)螫合劑,bathocuproine共同反應情形下,能抑制Cu(II)與4-ClCAT誘發的核酸損害作用,一結果顯示Cu(I)與活潑性氧分子中之H2O2可能為實際參與核酸損害作用之物種。此外,glutatione(GSH)亦可抑制 Cu(II)與4-ClCAT所誘發的DNA SSB及AP sites之生成,此一研究證據顯示,GSH可能是與4-ClCAT結合後中斷其氧化還原之環,終止ROS生成,進而抑制核酸損害作用,同時GSH亦有可能是直接與ROS反應,直接移除ROS,遠到保護DNA之作用。總結上述之實驗證據,如同對位?類化物,氯酚之鄰位?類物亦可經由不斷之氧化還原循環(redox cycle)生成H2O2,並對DNA造成氧化損害作用。
DNA damage induced by 4-chlorocatechol (4-ClCAT) was investigated using calf thymus DNA (ct-DNA) under physiological conditions. Results indicated that with the addition of transition metal copper (II) (20-100μM), parallel increases in DNA strand breaks and abasic (AP) sites were detected in ct-DNA exposed to 4-ClCAT(0.1-100μM) over the corresponding control. In the presence of both Cu(II) (20μM) and NADPH (100μM), 4-ClCAT induce a 100-fold increase in the number of AP sites at nanomolar concentration under physiological conditions. Further investigation indicated that the DNA damage induced by 4-ClCAT plus Cu(II) and NADPH was inhibited by the additons of catalase, copper(I)-specific chelator, and glutathione whereas superoxide dismutase and hydroyl radical scavengers were ineffective. These results suggest the involvement of Cu(I) and hydrogen peroxide in the induction of oxidative DNA damage by 4-ClCAT. In summary, these data demonstrate that similar to the para-quinonoid counterparts, chlorinated ortho-quinonoids are capable of inducing significant oxidative modifications in genomic DNA.
Relation: 興大工程學刊, Volume 13, Issue 3, Page(s) 201-209.
Appears in Collections:[期刊-興大工程學刊(原興大工程學報)] 第13卷 第3期
[依教師分類] 林伯雄

Files in This Item:

File SizeFormat
142315-4.pdf769KbAdobe PDF355View/Open


 


學術資源

著作權聲明

本網站為收錄中興大學學術著作及學術產出,已積極向著作權人取得全文授權,並盡力防止侵害著作權人之權益。如仍發現本網站之數位內容有侵害著作權人權益情事者,請權利人通知本網站維護人員,將盡速為您處理。

本網站之數位內容為國立中興大學所收錄之機構典藏,無償提供學術研究與公眾教育等公益性使用。

聯絡網站維護人員:wyhuang@nchu.edu.tw,04-22840290 # 412。

DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU/NCHU Library IR team Copyright ©   - Feedback