Rodríguez-Aguilera J C, Navas P
Departamento de Biología Celular, Facultad de Ciencias, Universidad de Córdoba, Spain.
J Bioenerg Biomembr. 1994 Aug;26(4):379-84. doi: 10.1007/BF00762778.
Ascorbate is stabilized in the presence of HL-60 cells. This stabilization has been questioned as a simple chemical effect. Further properties and controls about the enzymatic nature of this stabilization are described and discussed. Our results showed that cAMP derivatives and cAMP-increasing agents stimulated the ability of HL-60 cells to stabilize ascorbate. On the other hand, tunicamycin, a glycosylation-interfering agent, inhibited this ability. These data, together with hormonal regulation, support the hypothesis of an enzymatic redox system located at the plasma membrane as being responsible for the extracellular ascorbate stabilization by HL-60 cells.
抗坏血酸盐在HL - 60细胞存在的情况下得以稳定。这种稳定性曾被质疑只是一种简单的化学效应。本文描述并讨论了关于这种稳定性的酶促性质的进一步特性及对照实验。我们的结果表明,环磷酸腺苷(cAMP)衍生物和增加cAMP的试剂刺激了HL - 60细胞稳定抗坏血酸盐的能力。另一方面,衣霉素,一种干扰糖基化的试剂,抑制了这种能力。这些数据,连同激素调节,支持了位于质膜上的酶促氧化还原系统假说,该假说认为该系统负责HL - 60细胞对细胞外抗坏血酸盐的稳定作用。