Cantoni O, Brandi G, Salvaggio L, Cattabeni F
Ann Ist Super Sanita. 1989;25(1):69-73.
The molecular mechanisms of H2O2 toxicity have been investigated in both mammalian or bacterial cells. DNA breakage mediates cytotoxicity by low concentrations of H2O2 in mammalian cells, but DNA lesions do not appear as a direct consequence of the action of the hydroxyl radical; rather, these radicals may disturb intracellular Ca2+ homeostasis, which results in secondary reactions ultimately leading to DNA strand breakage and cytotoxicity. Studies that have used Escherichia coli (E. coli) as a cellular system have indicated that the two modes of killing detectable in cells exposed to increasing concentrations of H2O2 are mediated by different radical species. Mode-one killing seems to be produced by the superoxide anion whereas mode-two killing seems to be a consequence of the hydroxyl radical attack.
过氧化氢（H2O2）毒性的分子机制已在哺乳动物细胞和细菌细胞中进行了研究。在哺乳动物细胞中，低浓度的H2O2通过DNA断裂介导细胞毒性，但DNA损伤并非羟基自由基作用的直接后果；相反，这些自由基可能会扰乱细胞内Ca2+稳态，从而导致最终导致DNA链断裂和细胞毒性的次级反应。以大肠杆菌（E. coli）作为细胞系统的研究表明，在暴露于浓度不断增加的H2O2的细胞中可检测到的两种杀伤模式是由不同的自由基种类介导的。模式一的杀伤似乎是由超氧阴离子产生的，而模式二的杀伤似乎是羟基自由基攻击的结果。
