- 作者： 邱宗傑; 周玥岑; 曾婉芳
- 作者服務機構： 台北榮民總醫院內科部腫瘤科; 輔仁大學生物系
- 中文摘要：
本研究以人類肝癌細胞Hep G2和Hep 3B，及人類白血病細胞CCRF-CEM和MOLT-3探討脂質過氧化作用，麩胱
甘?（glutathione）及細胞內鈣離子濃度在維他命 (方程式無法摘錄) 引發之細胞毒性中扮演的角色。維他命 (方程式無法摘錄) 導致細胞死亡前，細胞
內麩胱甘?含量降低，細胞內鈣離子濃度及脂質過氧化作用增加。細胞對維他命 (方程式無法摘錄) 之敏感度依序為Hep G2 > Hep 3B >
CCRF-CEM和MOLT-3。維他命 (方程式無法摘錄) 引發此些細胞脂質過氧化作用增加之次序與細胞對維他命 (方程式無法摘錄) 之敏感度相同。
維他命 (方程式無法摘錄) 引發細胞內麩胱甘?含量降低之先後為Hep G2 > MOLT-3及CCRF-CEM > Hep 3B。維他命 (方程式無法摘錄) 引發細胞內鈣
離子濃度增加依序為Hep G2 > MOLT-3 > CCRF-CEM及Hep 3B。Hep G2細胞先和鐵離子結合劑（deferoxamine
mesylate）作用，可降低維他命 (方程式無法摘錄) 引發之細胞死亡及脂質過氧化作用，但對維他命 (方程式無法摘錄) 引發綑胞內麩胱甘?含量降低
及細胞內鈣離子濃度增加則無影響。此些數據顯示維他命 (方程式無法摘錄) 之細胞毒性和其引發之脂質過氧化作用有直接相關，而
和其引發之細胞內鈣離子濃度增加及麩胱甘?減少較不直接相關。Dicumarol（DT-diaphorase之抑制劑）會增進維他命
(方程式無法摘錄) 對Hep 3B細胞之毒性，細胞在37℃和維他命 (方程式無法摘錄) 作用120分鐘，細胞死亡由73.1%增加為86.2%，但對Hep G2, CCRF-
CEM及MOLT-3細胞之毒性則無影響。DT-diaphorase之活性在Hep G2, Hep 3B, CCRF-CEM及MOLT-3細胞分別為52.4,
39.6,1.5及1.8 nmol cytochrome c reduced/min/mg protein。Hep G2細胞之DT-diaphorase活性較其他細胞為高。本實驗顯
示DT-diaphorase並無法如其他研究者所預期的，保護細胞免於維他命 (方程式無法摘錄) 之毒性。
0 - 英文摘要： The role of lipid peroxidation, intracellular glutathione and (方程式無法摘錄) concentration in menadione-medi-ated toxicity was investigated in human hepatoma cell lines, Hep G2 and Hep 3B, and in human leukemia celllines, CCRF-CEM and MOLT-3. Incubation of these cells with 80 μM menadione at 37℃ resulted in deple-tion of intracellular glutathione, increased intracellular (方程式無法摘錄), and increased lipid peroxidation, events leadingto cell degeneration. The sensitivity of these cells to menadione, in order, was: Hep G2 cells > Hep 3B cells >CCRF-CEM cells and MOLT-3 cells. The extent of menadione-induced lipid peroxidation in different celltypes followed the same order as did their susceptibility to menadione-induced cell degeneration. The mena-dione-induced depletion in glutathione level was in the following sequence: Hep G2 cells > MOLT-3 andCCRF-CEM cells > Hep 3B cells. The extent of the menadione-induced increase in the intracellular (方程式無法摘錄) concentration was: Hep G2 cells > Molt-3 cells > CCRF-CEM cells and Hep 3B cells. Pre-treatment ofHep G2 cells with 20 mM deferoxamine mesylate, an iron chelator, reduced both the menadione-inducedcell degeneration and lipid peroxidation; however, it did not prevent the menadione-induced increase inintracellular (方程式無法摘錄) nor the depletion of glutathione. These data suggest that menadione-induced celldegeneration is directly linked to lipid peroxidationa, and that it is less related to the rise in intracellular (方程式無法摘錄)and the depletion in glutathione content. Dicumarol (an inhibitor of DT diaphorase) enhanced thecapacity of menadione to induce Hep 3B cell degeneration from 71.3% to 86.2% after 120 min ofmenadione treatment at 37℃, but did not have this effect in Hep G2, CCRF-CEM or MOLT-3 cells. Theactivities of DT diaphorase were 52.4, 39.6, 1.5 and 1.8 nmol cytochrome c reduced/min/mg protein in Hep G2,Hep 3B, CCRF-CEM and MOLT-3 cells, respectively. The activity of DT diaphorase was much higher inHep G2 cells than in the other cells. It seems that DT diaphorase may not, as suggested by others,protect against cell degeneration by quinones, such as menadione.
- 中文關鍵字： menadione;lipid peroxidation; intracellular Ca2+; gluathione.
- 英文關鍵字： --
