Kong S, Davison A J, Bland J
Int J Radiat Biol Relat Stud Phys Chem Med. 1981 Jul;40(1):19-29.
With respect to both permeability and inactivation of membranous GAPDH, ghosts were more susceptible than erythrocytes to free radicals produced in the gamma-irradiation of aqueous solutions. The rate of increase in the permeability of irradiated ghosts was immeasurably greater than that of irradiated erythrocytes, while the rate of inactivation of GAPDH was 21-fold greater. The sensitivity of ghosts to radiation damage was affected strongly by the presence of oxygen during irradiation. In the presence of air, the rates of increase of permeability and inactivation of GAPDH were 2.8- and 1.5-fold of those in the presence of N2. The use of buffer saturated with oxygen accelerated the aerobic rates of increase of permeability and inactivation of GAPDH by 60- and 2.7-fold. These results indicate that inactivation of GAPDH is somewhat sensitive to oxygen, particularly at high concentration of oxygen. Nevertheless, in air or under nitrogen, the rate of enzymic inactivation was almost an order of magnitude greater than that of increase of permeability, indicating that the former is much more sensitive to irradiation. The major mechanism of the oxygen effect observed is the ability of oxygen to increase the branching of the free radical chain reactions which propagate damage after initiation within the membrane.
关于膜结合甘油醛 - 3 - 磷酸脱氢酶(GAPDH)的通透性和失活,红细胞影比红细胞对水溶液γ辐射产生的自由基更敏感。辐照红细胞影的通透性增加速率比辐照红细胞的增加速率大得无法测量,而GAPDH的失活速率则大21倍。红细胞影对辐射损伤的敏感性在辐照过程中受氧气存在的强烈影响。在空气中,GAPDH的通透性增加速率和失活速率分别是在氮气中时的2.8倍和1.5倍。使用饱和氧气的缓冲液使GAPDH的需氧通透性增加速率和失活速率分别加快60倍和2.7倍。这些结果表明,GAPDH的失活对氧气有些敏感,尤其是在高浓度氧气时。然而,在空气或氮气环境下,酶失活速率几乎比通透性增加速率大一个数量级,表明前者对辐照更敏感。观察到的氧气效应的主要机制是氧气能够增加自由基链反应的分支,这些自由基链反应在膜内引发损伤后传播损伤。