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研究生:郭順利
研究生(外文):ShunLi Kuo
論文名稱:過氧化氫致使大鼠心室細胞胞內離子失衡之可能機制探討
論文名稱(外文):Possible mechanisms of hydrogen peroxide induced intracellular ion disturbance in rat cardiomyoctes
指導教授:吳美玲吳美玲引用關係
指導教授(外文):Wu, Mei-Lin
學位類別:碩士
校院名稱:國立臺灣大學
系所名稱:生理學研究所
學門:醫藥衛生學門
學類:醫學學類
論文種類:學術論文
論文出版年:2001
畢業學年度:89
語文別:中文
論文頁數:74
中文關鍵詞:心臟心肌細胞自由基鈣離子鈉離子酸化幼鼠過氧化氫
外文關鍵詞:heartcardiomyocytefree radicalcalciumsodiumacidosisneonatalhydrogen peroxide
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超氧自由基 (O2-‧)、氫氧自由基 (‧OH) 等的含氧自由基被證實能引起心臟的許多病理異常。心臟遭受自由基攻擊後,會導致stunning、心肌梗塞及心臟衰竭等。一般認為,在缺血再灌流 (ischemia reperfusion) 後產生的鈣離子大量上升(calcium overload),其後活化caspases而引起apoptosis,是造成缺血再灌流傷害的重要原因。然而,造成calcium overload 的機制至今仍未闡明。本實驗中,我們使用過氧化氫產生含氧自由基來研究自由基造成胞內離子失衡的機制,並且利用BCECF、fura-2及SBFI量測心室細胞內酸鹼度、鈣離子及鈉離子的濃度的變化。加入H2O2 (100 M) 能引起心室細胞的鈣離子及鈉離子大量上升,並造成胞內酸化。而這種現象能被phenanthroline 及 deferoxamine 這兩種胞內鐵鉗合劑所完全阻斷。由於H2O2經鐵離子催化能產生‧OH,這些結果顯示了‧OH是造成Ca2+/Na+ overload元凶。更進一步的利用xanthine oxdidase和 hypothanxine 來產生O2-‧與‧OH,我們也發現了類似的Ca2+/Na+ overload。並且此作用主要是透過‧OH 而來。‧OH引起的 calcium overload其鈣離子來源主要來自胞外,粒線體釋出的鈣離子可能也是來源之一。就我們所知,由‧OH引起胞外鈣離子進入細胞的途徑並非經由 (i). 已知之Ca2+ leak channel (ii) 抑制 Ca2+-ATPase (iii) L-type Ca2+ channel (iv) 活化 PLA2s 裂解細胞膜,所造成之non-specific 的離子漏入等機制而來。雖然melittin (能活化PLA2 )、花生四烯酸 (arachidonic acid)及lysophosphatidyl choline (均為PLA2活化後產物) 都能引起鈣離子上升。但因處理H2O2後,AA的釋放在24小時有持續增加的趨勢,因此,PLA2引起細胞離子失衡,可能出現在較後時期。最後,至於鈉鈣離子交換的逆轉模式是否是引起鈣離子上升的原因,需要再進一步證實。至於鈉離子進入細胞則可能透過Na+-H+ exchange或者non-specific 的cation leak而來。藉著使用rhodamine 123來量測粒線體的膜電位 (m) 變化,我們發現H2O2能引起 m 的hyperpolarization,但這結果需要進一步驗證。綜合以上證據,我們發現在大鼠心室細胞中,‧OH是造成胞內離子失衡的主因,鈣離子的上升主要來自胞外,胞內粒線體釋放也佔了其中一部份,而胞外鈣離子進入的途徑可能經由鈉鈣離子交換的逆轉模式或者non-specific 的cation leak,但此種channel尚未有任何已知之抑制劑可以抑制。自由基造成鈉離子上升則可能經由類似的non-specific cation leak或者Na+-H+ 交換而來。這些離子的失衡可能導致心臟的病理異常。

Oxygen free radicals have been shown to induce pathological effects in hearts. A marked increase in free radicals results in myocardiac stunning , infarction and heart failure. It is suggested that free radicals induce calcium overload and subsequent caspases activation may play an important role in ischemia reperfusion injury. However, possible mechanisms responsible for this calcium overload are not clearly elucidated. To investigate possible mechanisms of free radical induced intracellular ion disturbance, we use hydrogen peroxide (H2O2) as a means to generate oxygen free radicals, and use BCECF , fura-2 and SBFI, respectively, to measure intracellular pH (pHi), calcium ([Ca2+]i) or sodium ([Na+]i) in primary culture of rat cardiomyocytes. Addition of H2O2 (100 M) induced calcium overload, sodium overload, and an intracellular acidification in rat cardiomyocytes. The Ca2+/Na+ overload can be completely bolcked by intracellular iron chelators. Since it is known that‧OH can be produced by ferrous iron catalysis of H2O2 . These results indicate that Ca2+/Na+ overload were induced by‧OH. Further, xanthine oxdidase and hypoxanthine were used to generate both O2-‧and‧OH, similar Ca2+/Na+ overload were again seen. The calcium resources of‧OH-induced calcium overload may mainly due to influx of extracellular calcium, though calcium released by mitochondria may also play a role. To our best knowledge, possible pathways for‧OH induced extracellular Ca2+ influx were not through (i). Ca2+ leak channel (ii) inhibition of Ca2+-ATPase (iii) L-type Ca2+ channel (iv) activated PLA2s resulting in membrane degradation and then induced non-specific ions leak. However, melittin (PLA2 activator), arachidonic acid (AA) and lysophosphatidyl choline (both are PLA2 products) induce calcium overload. Besides, AA release increases after H2O2 treatment. Thus, PLA2 prabably induce intracellular ion imbalance in the later periods. At last, whether calcium overload is induced by a reverse mode of the Na+-Ca2+ exchange needs to be further confirmed. Possible mechanisms responsible for free radical induced sodium overload may be (i). Non specific cation leak (ii). Na+-H+ exchange. We also found that H2O2 induces m hyperpolarization. Further studies regarding the connection between m changes and calcium release of mitochondria need to be investigated.

圖次 . . . . . . . . . . . . . . .. . . . . . . . . . . .IV
表次 . . . . . . . . . . . . . . . . . . . . . . . . . .V
中文摘要 . . . . . . . . . . . . . .. . . . . . . . . . .VI
英文摘要 . . . . . . . . . . . . . . . . . . . . . . . . VII
緒論 . . . . . . . . . . . . . . . . . . . . . . . . . . 1
材料與方法 . . . . . . . . . . . . . . . . . . . . . . . 14
結果 . . . . . . . . . . . . . . . . . . . . . . . . . . 24
討論 . . . . . . . . . . . . . . . . . . . . . . . . . . 34
結論 . . . . . . . . . . . . . . . . . . . . . . . . . . 46
圖表 . . . . . . . . . . . . . . . . . . . . . . . . . .47
參考文獻 . . . . . . . . .. . . . . . . . . . . . . . . .66

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