Wefers H, Sies H
Eur J Biochem. 1983 Dec 1;137(1-2):29-36. doi: 10.1111/j.1432-1033.1983.tb07791.x.
The reaction of superoxide with reduced glutathione (GSH) was studied with two O-.2-producing systems: xanthine oxidase using xanthine or acetaldehyde as substrates, and secondly, quinol autoxidation. The capability of GSH to quench superoxide radicals was detected by lowered O-.2-mediated cytochrome c3+ reduction. The formation of the oxidation products, glutathione disulfide (GSSG) and glutathione sulfonate (the latter at levels of about 6-15% compared to GSSG), was dependent on the O-.2 production and was inhibited by superoxide dismutase. The presence of GSH together with an O-.2-producing system led to an extra uptake of oxygen, which was also depressed by superoxide dismutase. The observed O2 uptake was accounted for by the formation of GSSG and GSO-3 from GSH; the data are in accordance with a mechanism involving thiyl radicals. Low-level chemiluminescence measurement indicated the formation of excited oxygen species. The intensity of photoemission was dependent on the GSH concentration and on the O-.2 production rate. Chemiluminescence was inhibited by superoxide dismutase and also by glutathione peroxidase, but not by catalase or OH. quenchers. Spectral analysis and the effects of 1,4-diazabicyclo[2.2.2]octane and sodium azide indicated the contribution of singlet molecular oxygen to the light emission. It is suggested that singlet oxygen results from an intermediate oxygen addition product such as a glutathione peroxysulphenyl radical.
利用两个产生超氧阴离子(O₂⁻)的系统研究了超氧阴离子与还原型谷胱甘肽(GSH)的反应:以黄嘌呤或乙醛为底物的黄嘌呤氧化酶系统,以及其次的喹啉自氧化系统。通过降低O₂⁻介导的细胞色素c³⁺还原检测GSH淬灭超氧阴离子自由基的能力。氧化产物谷胱甘肽二硫化物(GSSG)和谷胱甘肽磺酸酯(后者与GSSG相比含量约为6 - 15%)的形成取决于O₂⁻的产生,并受到超氧化物歧化酶的抑制。GSH与产生O₂⁻的系统共存导致额外的氧气摄取,这也受到超氧化物歧化酶的抑制。观察到的氧气摄取是由GSH形成GSSG和GSO₃⁻所致;数据符合涉及硫自由基的机制。低水平化学发光测量表明形成了激发态氧物种。光发射强度取决于GSH浓度和O₂⁻产生速率。化学发光受到超氧化物歧化酶以及谷胱甘肽过氧化物酶的抑制,但不受过氧化氢酶或羟基自由基淬灭剂的抑制。光谱分析以及1,4 - 二氮杂双环[2.2.2]辛烷和叠氮化钠的作用表明单线态分子氧对发光有贡献。有人认为单线态氧来自中间的氧加成产物,如谷胱甘肽过氧亚磺酰基自由基。