Koh W S, Lee S J, Lee H, Park C, Park M H, Kim W S, Yoon S S, Park K, Hong S I, Chung M H, Park C H
Department of Medicine, Samsung Medical Center, Kangnam-ku Seoul, Korea.
Anticancer Res. 1998 Jul-Aug;18(4A):2487-93.
In order to investigate the differential effects of ascorbate derivatives on leukemic cell growth, we examined their stabilities and transmembrane transport efficiencies. The growth of HL-60 and U937 cells was dose-dependently inhibited by ascorbic acid and sodium ascorbate, but not by dehydroascorbic acid and magnesium ascorbyl 2-phosphate up to 200 microM. The growth-suppression by ascorbic acid was dependent on its redox state, showing a complete or partial reversion by ascorbate oxidase or FeCl3 addition, respectively. Three different patterns of intracellular ascorbic acid accumulation were observed by HPLC according to the species of ascorbate derivative applied for the incubation. Compared with the reduced form of ascorbic acid, the oxidized forms (dehydroascorbic acid, ascorbic acid plus ascorbate oxidase or FeCl3) were rapidly transported into cells and readily degraded, while magnesium ascorbyl 2-phosphate, a stable derivative of ascorbic acid, slowly elevated the intracellular level of ascorbic acid, reaching a plateau at 24 hours. We also measured the differential kinetics of ascorbic acid levels In culture supernatants following the addition of ascorbate derivatives. Ascorbic acid at 40, 10, or 1 microM was observed 3 hours following treatment with 100 microM of ascorbic acid, ascorbic acid plus FeCl3, or magnesium ascorbyl 2-phosphate, respectively. No ascorbic acid was found in the culture supernatant treated with dehydroascorbic acid. This order of ascorbic acid concentrations in culture supernatant reflects their growth-inhibitory effects. Thus the growth inhibitory effect of ascorbic acid appears to be dependent on its concentration in culture medium rather than its intracellular concentration. In conclusion, the results in this study indicate that the differential effects of ascorbate derivatives appear to be due to the actual concentration differences of the reduced form of ascorbic acid in culture medium following their addition, which is determined by their stability and efficiency of cellular uptake.
为了研究抗坏血酸衍生物对白血病细胞生长的不同影响,我们检测了它们的稳定性和跨膜转运效率。高达200微摩尔时,抗坏血酸和抗坏血酸钠对HL-60和U937细胞的生长有剂量依赖性抑制作用,但脱氢抗坏血酸和抗坏血酸镁2-磷酸酯则无此作用。抗坏血酸的生长抑制作用取决于其氧化还原状态,分别添加抗坏血酸氧化酶或FeCl3后,其抑制作用会完全或部分逆转。根据用于孵育的抗坏血酸衍生物种类,通过高效液相色谱法观察到细胞内抗坏血酸积累有三种不同模式。与抗坏血酸的还原形式相比,氧化形式(脱氢抗坏血酸、抗坏血酸加抗坏血酸氧化酶或FeCl3)能迅速转运到细胞内并易于降解,而抗坏血酸的稳定衍生物抗坏血酸镁2-磷酸酯则能缓慢提高细胞内抗坏血酸水平,在24小时时达到平台期。我们还测量了添加抗坏血酸衍生物后培养上清液中抗坏血酸水平的差异动力学。分别用100微摩尔抗坏血酸、抗坏血酸加FeCl3或抗坏血酸镁2-磷酸酯处理3小时后,在培养上清液中观察到40、10或1微摩尔的抗坏血酸。用脱氢抗坏血酸处理的培养上清液中未发现抗坏血酸。培养上清液中抗坏血酸浓度的这种顺序反映了它们的生长抑制作用。因此,抗坏血酸的生长抑制作用似乎取决于其在培养基中的浓度而非细胞内浓度。总之,本研究结果表明,抗坏血酸衍生物的不同作用似乎是由于添加后培养基中抗坏血酸还原形式的实际浓度差异所致,而这种差异由它们的稳定性和细胞摄取效率决定。