Ueda J, Saito N, Ozawa T
National Institute of Radiological Sciences, Chiba-shi, Japan.
Arch Biochem Biophys. 1996 Jan 1;325(1):65-76. doi: 10.1006/abbi.1996.0008.
Using 5,5-dimethyl-1-pyrroline N-oxide (DMPO) as a spin trap, alkoxyl radicals and peroxyl radicals produced from the reactions of tert-butyl hydroperoxide(tBuOOH) and cumene hydroperoxide (PhC(CH3)2OOH) with some copper(Cu)(II) complexes such as Cu(II) complexes of cimetidine (Cim), cyclo(L-histidyl-L-histidyl) (CyHH), L-histidylglycine (HG), and L-histidylglycylglycine (HGG) were detected by electron spin resonance (ESR) spectroscopy. However, Cu(II) complexes of glycyl-L-histidine (GH), glycyl-L-histidylglycine (GHG),glycylglycyl-L-histidine (GGH), and glycylglycyl-L-histidyl-glycine (GGHG) did not cause the generation of free radicals during the reaction with tert-butyl or cumene hydroperoxide. Addition of a biological reductant such as cysteine or glutathione to the system including these Cu(II) complexes and hydroperoxides gave tert-butoxyl and cumyl alkoxyl (RO.) radicals, respectively. These alkoxyl radicals underwent subsequent beta-scission reaction and generated the carbon-centered radical (R.). Although cysteine and glutathione are considered to be cellular antioxidants, our results suggest that these biological reductants facilitate Cu(II) complexes-dependent free radical generation.
以5,5-二甲基-1-吡咯啉N-氧化物（DMPO）作为自旋捕获剂，通过电子自旋共振（ESR）光谱检测了叔丁基过氧化氢（tBuOOH）和氢过氧化异丙苯（PhC(CH3)2OOH）与一些铜（Cu）（II）配合物（如西咪替丁（Cim）、环（L-组氨酰-L-组氨酰）（CyHH）、L-组氨酰甘氨酸（HG）和L-组氨酰甘氨酰甘氨酸（HGG）的Cu（II）配合物）反应产生的烷氧基自由基和过氧自由基。然而，甘氨酰-L-组氨酸（GH）、甘氨酰-L-组氨酰甘氨酸（GHG）、甘氨酰甘氨酰-L-组氨酸（GGH）和甘氨酰甘氨酰-L-组氨酰甘氨酸（GGHG）的Cu（II）配合物在与叔丁基过氧化氢或氢过氧化异丙苯反应过程中不会产生自由基。向包含这些Cu（II）配合物和氢过氧化物的体系中添加生物还原剂（如半胱氨酸或谷胱甘肽），分别产生叔丁氧基和异丙苯基烷氧基（RO.）自由基。这些烷氧基自由基随后发生β-断裂反应并生成碳中心自由基（R.）。尽管半胱氨酸和谷胱甘肽被认为是细胞抗氧化剂，但我们的结果表明，这些生物还原剂促进了Cu（II）配合物依赖性自由基的产生。
