Alcaín F J, Burón M I, Rodríguez-Aguilera J C, Villalba J M, Navas P
Departamento de Biología Celular, Facultad de Ciencias, Universidad de Córdoba, Spain.
Cancer Res. 1990 Sep 15;50(18):5887-91.
Ascorbate free radical stimulates the growth of human promyelocytic leukemia cells (HL-60) in the presence of a limited amount of serum (1%) when added to the cells under conditions where it is impermeable. Maximum growth stimulation occurs at concentrations from 5 x 10(-9) to 2 x 10(-8) M. Ascorbate mimicks the stimulation effect of its free radical but stimulates at higher concentrations. Autoxidation of ascorbate by oxygen produces its free radical, which apparently causes growth stimulation. Ascorbate could be regenerated by intact cells in vitro, since prevention of autoxidation of ascorbate in the presence of cells is observed. Neither dehydroascorbate nor isoascorbate increases HL-60 cell growth. Short term incubation of cells in the presence of ascorbate free radical induced intracellular NADH oxidation. We propose that the stimulation of growth of HL-60 cells shown here could be caused by activation of the transplasma membrane electron transport system by the ascorbate free radical.
在存在有限量血清(1%)的情况下,当抗坏血酸自由基在不可渗透的条件下添加到细胞中时,它会刺激人早幼粒细胞白血病细胞(HL-60)的生长。最大生长刺激发生在浓度为5×10⁻⁹至2×10⁻⁸ M时。抗坏血酸模拟其自由基的刺激作用,但在更高浓度下才会产生刺激。抗坏血酸被氧气自动氧化产生其自由基,这显然导致了生长刺激。抗坏血酸可以在体外被完整细胞再生,因为在细胞存在的情况下观察到抗坏血酸的自动氧化被阻止。脱氢抗坏血酸和异抗坏血酸都不会增加HL-60细胞的生长。在抗坏血酸自由基存在的情况下对细胞进行短期孵育会诱导细胞内NADH氧化。我们提出,此处所示的HL-60细胞生长刺激可能是由抗坏血酸自由基激活跨质膜电子传递系统引起的。