- 作者: 曾婉芳; 邱宗傑; 黃仁奕; 陳義雄
- 作者服務機構: 輔仁大學生物系; 臺北榮民總醫院內科部腫瘤科; 國立臺灣大學生化科學研究所及中央研究院生化研究所
- 中文摘要:
為了解維他命K 是否具心臟毒性,本研究利用新生大白鼠心肌細胞探討維他命K 對心肌細胞之跳動,細胞內腺
?三磷酸和鈣離子濃度及細胞存活之影響。結果發現維他命K 會使細胞跳動變慢,繼而停止。細胞表面有小泡(bleb)出
現,終至鈿胞死亡。維他命K 導致細胞跳動變慢的時候,鈿胞內腺?三磷酸有明顯的減少,而鈣離子之濃度則有明顯
增加。如果在小泡出現前,將未進入細胞內之維他命K 除去,則細胞可存活,且大部分細胞回復規律性之跳動。以
diltiazem(乃鈣離子拮抗劑)或fura-2 acetoxymethyl ester(乃鈣離子結合劑)或antipain(蛋白?抑制劑)先處理細胞
則可抑制維他命K 之毒性。本研究顯示維他命K 具心臟毒性,且其導致心肌細胞內鈣離子濃度之增加和其心臟毒性
有關。
i - 英文摘要: Cardiotoxicity of menadione was elucidated in neonatal rat cardiomyocytes. When incubated withmenadione, contraction of myocytes initially slowed down and eventually stopped. Later blebs appearedon the cell surface, leading to cell degeneration. During the time of diminished cellular contraction, a largeportion of endogenous ATP was depleted whilst intracellular Ca levels were increased. However, ifmenadione was washed out prior to termination of contraction, the myocytes survived and most of thecells resumed regular contraction. Preincubation of the cells with diltiazem (a Ca antagonist), or fura-2acetoxymethyl ester (a chelate for Ca ), or antipain (a proteinase inhibitor) suppressed menadione's abilityfor cellular damage. These results indicate that menadione is toxic to cardiomyocytes, and that the increaseof intracellular Ca is related to the mechanism of cardiotoxicity of menadione.
- 中文關鍵字: menadione; cardiotoxicity; intracellular Ca2+.
- 英文關鍵字: --