Bors W, Michel C, Dalke C, Stettmaier K, Saran M, Andrae U
Institut für Strahlenbiologie and Institut für Toxikologie, GSF Forschungszentrum für Umwelt und Gesundheit, Neuherberg, FRG.
Chem Res Toxicol. 1993 May-Jun;6(3):302-9. doi: 10.1021/tx00033a008.
The chemistry of the nonenzymatic oxidation of the rat liver carcinogen, 2-nitropropane, and its anionic form, propane-2-nitronate, was investigated using pulse radiolysis and EPR/spin trapping with 3,5-dibromo-4-nitrosobenzenesulfonic acid as the trapping agent. The results suggest that, following initial oxidation to a secondary alkyl radical, propane-2-nitronate is effectively degraded in a peroxidative chain reaction with the intermediary formation of peroxyl and NO2.radicals. The latter radical was shown to react appreciably fast with ribonucleosides, deoxyribonucleosides, and guanosine nucleotides. It is proposed that nonenzymatic formation of NO2.radicals after enzymatic oxidation of propane-2-nitronate to the corresponding secondary alkyl radical accounts for the induction of DNA damage observed after exposure of rats to 2-nitropropane.
使用脉冲辐解和以3,5-二溴-4-亚硝基苯磺酸为俘获剂的电子顺磁共振/自旋俘获技术，研究了大鼠肝脏致癌物2-硝基丙烷及其阴离子形式2-硝基丙烷阴离子的非酶促氧化化学过程。结果表明，2-硝基丙烷阴离子在初步氧化为仲烷基自由基后，在过氧化物链式反应中有效降解，中间形成过氧自由基和二氧化氮自由基。已证明后一种自由基与核糖核苷、脱氧核糖核苷和鸟苷核苷酸反应相当迅速。有人提出，2-硝基丙烷阴离子经酶促氧化生成相应的仲烷基自由基后，非酶促形成二氧化氮自由基，这是大鼠接触2-硝基丙烷后观察到的DNA损伤诱导的原因。
