Imlay J A, Chin S M, Linn S
Department of Biochemistry, University of California, Berkeley 94720.
Science. 1988 Apr 29;240(4852):640-2. doi: 10.1126/science.2834821.
Exposure of Escherichia coli to low concentrations of hydrogen peroxide results in DNA damage that causes mutagenesis and kills the bacteria, whereas higher concentrations of peroxide reduce the amount of such damage. Earlier studies indicated that the direct DNA oxidant is a derivative of hydrogen peroxide whose formation is dependent on cell metabolism. The generation of this oxidant depends on the availability of both reducing equivalents and an iron species, which together mediate a Fenton reaction in which ferrous iron reduces hydrogen peroxide to a reactive radical. An in vitro Fenton system was established that generates DNA strand breaks and inactivates bacteriophage and that also reproduces the suppression of DNA damage by high concentrations of peroxide. The direct DNA oxidant both in vivo and in this in vitro system exhibits reactivity unlike that of a free hydroxyl radical and may instead be a ferryl radical.
将大肠杆菌暴露于低浓度过氧化氢会导致DNA损伤，进而引起诱变并杀死细菌，而较高浓度的过氧化物会减少此类损伤的数量。早期研究表明，直接的DNA氧化剂是过氧化氢的一种衍生物，其形成依赖于细胞代谢。这种氧化剂的产生取决于还原当量和一种铁物种的可用性，它们共同介导芬顿反应，其中亚铁离子将过氧化氢还原为活性自由基。建立了一种体外芬顿系统，该系统会产生DNA链断裂并使噬菌体失活，同时也能重现高浓度过氧化物对DNA损伤的抑制作用。体内和该体外系统中的直接DNA氧化剂均表现出与游离羟基自由基不同的反应活性，可能是一种高铁自由基。
