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| 題 名 | Menadione-Induced Cell Degeneration is Related to Lipid Peroxidation in Human Cancer Cells=維他命K[feb0]引發人類癌細胞之死亡和脂質過氧化作用有關 |
|---|---|
| 作 者 | 邱宗傑; 周玥岑; 曾婉芳; | 書刊名 | Proceedings of the National Science Council : Part B, Life Science |
| 卷 期 | 22:1 1998.01[民87.01] |
| 頁 次 | 頁13-21 |
| 分類號 | 415.138 |
| 關鍵詞 | 維他命K[feb0]; 人類癌細胞; 細胞死亡; 脂質過氧化作用; Menadione; Lipid peroxidation; Intracellular Ca[fec7]; Glutathione; |
| 語 文 | 英文(English) |
| 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 探討脂質過氧作用, 麩胱甘 ( glutathione )及細胞鈣離子濃度在維他命 K �� 引發之細胞毒性中扮演的角色。 維他命 K �偏伬P細胞死亡前,細胞肉麩胱甘 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 K �陘妤虓P度依序為 Hep G2>Hep 3B>CCRF-CEM 和 MOLT-3。維他命 K �陘瑑o此些細胞脂質過氧化作用增加之次序與細胞對維 他命 K �陘妤虓P度相同。維他命 K �陘瑑o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 K �陘瑑o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 K �陘瑑o細胞死亡及脂質過氧化作用,但對維他命 K �� 引發細胞內麩胱甘�顜t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 K �陘妓茩M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 K �偎� Hep 3B 細胞之毒性,細胞在 37 ℃和維他命 K �飢@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 Hap 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 K �陘妞r性。 |
| 英文摘要 | The role of lipid peroxidation, intracellular glutathione and Ca �� concentration in menadione-mediated toxicity was investigated in human hepatoma cell lines, Hep G2 and Hep 3B, and in human leukemia cell lines, CCRF-CEM and MOLT-3. Incubatin of these cells with 80 uM menadione at 37 ℃ resulted in depletion of intracellular glutathione, increased intracellular Ca ��, and increased lipid peroxidation, events leading to 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 cell types followed the same order as did their susceptibility to menadione-induced cell degeneration. The menadione-induced depletion in glutathione level was in the following sequence: Hep G2 cells>MOLT-3 and CCRF-CEM cells>Hep 3B cells. The extent of the menadione-induced increase in the intracellular Ca �� concentration was: Hep G2 cells > Molt-3 cells < CCRF-CEM cells and Hep 3B cells. Pre-treatment of Hep G2 cells with 20 mM deferoxamine mesylate, an iron chelator, reduced both the menadione-induced cell degeneration and lipid peroxidation; however, it did not prevent the menadinoe-induced increase in intracellular Ca �� nor the depletion of glutathione. These data suggest that menadione-induced cell degeneration is directly linked to lipid peroxidation, and that it is less related to the rise in intracellular Ca �� and the depletion in glutathione content. Dicumarol (and inhibitor of DT diaphorase) enhanced the capacity of menadione to induce Hep 3B cell degeneration from 71.3% to 86.2% after 120 min of menadione treatment at 37 ℃, but did not have this effect in Hep G2, CCRF-CEM or MOLT-3 cells. The activities 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 in Hep 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. |
本系統中英文摘要資訊取自各篇刊載內容。