Sakagami H, Kuribayashi N, Iida M, Hagiwara T, Takahashi H, Yoshida H, Shiota F, Ohata H, Momose K, Takeda M
First Department of Biochemistry, School of Medicine, Showa University, Tokyo, Japan.
Life Sci. 1996;58(14):1131-8. doi: 10.1016/0024-3205(96)00071-9.
The requirement for and mobilization of Ca2+ ions during induction of cell death by sodium ascorbate were compared with those during induction of cell death by hydrogen peroxide. When HL-60 cells were incubated with sodium ascorbate, a rapid increase in the intracellular concentration of Ca2+ ions and subsequent apoptotic cell death, characterized by cell shrinkage, nuclear fragmentation and cleavage of internucleosomal DNA to yield fragments that were multiples of 180-200 base pairs, were induced. However, these effects of sodium ascorbate were significantly reduced in Ca2+-depleted medium. By contrast, hydrogen peroxide induced similar apoptosis associated phenomena in the presence and in the absence of extracellular Ca2+ ions. The intracellular concentration of the reduced form of glutathione was not significantly affected and glutathione disulfide was undetectable during the early stages of apoptosis. These data suggest that sodium ascorbate and hydrogen peroxide initiate cell death by different mechanisms.
将抗坏血酸钠诱导细胞死亡过程中Ca2+离子的需求和动员情况与过氧化氢诱导细胞死亡过程中的情况进行了比较。当HL-60细胞与抗坏血酸钠一起孵育时，细胞内Ca2+离子浓度迅速增加，随后发生凋亡性细胞死亡，其特征为细胞收缩、核碎裂以及核小体间DNA断裂产生180 - 200碱基对倍数的片段。然而，在Ca2+耗尽的培养基中，抗坏血酸钠的这些作用显著降低。相比之下，无论有无细胞外Ca2+离子，过氧化氢均诱导出类似的凋亡相关现象。在凋亡早期，谷胱甘肽还原形式的细胞内浓度未受到显著影响，且未检测到谷胱甘肽二硫化物。这些数据表明，抗坏血酸钠和过氧化氢通过不同机制引发细胞死亡。
