Satoh K, Sakagami H
Analysis Center, School of Pharmaceutical Sciences, Showa University, Tokyo, Japan.
Anticancer Res. 1997 Mar-Apr;17(2A):1125-9.
Various metal ions were investigated for their ability to modify the radical intensity and cytotoxic activity of sodium ascorbate or ascorbic acid. The addition of metal ions, such as Cu+, Cu2+, Fe2+, Zn2+, Mn2+ and Fe3+, dose-dependently enhanced the ascorbyl radical intensity whereas Na+, K+, Ca2+ and Mg2+ were totally inactive. The enhancement of ascorbyl radical intensity by metal ions was tightly coupled with the accelerated degradation of ascorbate. Addition of either serum or albumin significantly reduced the stimulation effect of Cu2+, and almost completely eliminated that of Fe3+ and Zn2+. The noncytotoxic concentration of Cu2+ significantly enhanced the cytotoxicity of ascorbate against cultured human glioblastoma T98G cell line. The present data suggest the possible role of metal ions in the regulation of the biological activity of ascorbate.
研究了各种金属离子改变抗坏血酸钠或抗坏血酸的自由基强度和细胞毒性活性的能力。添加金属离子,如Cu+、Cu2+、Fe2+、Zn2+、Mn2+和Fe3+,剂量依赖性地增强了抗坏血酸自由基强度,而Na+、K+、Ca2+和Mg2+则完全无活性。金属离子对抗坏血酸自由基强度的增强与抗坏血酸的加速降解紧密相关。添加血清或白蛋白可显著降低Cu2+的刺激作用,几乎完全消除Fe3+和Zn2+的刺激作用。非细胞毒性浓度的Cu2+显著增强了抗坏血酸对培养的人胶质母细胞瘤T98G细胞系的细胞毒性。目前的数据表明金属离子在调节抗坏血酸生物活性中可能发挥的作用。