TOXIC DNA DAMAGE BY HYDROGEN-PEROXIDE THROUGH THE FENTON REACTION INVIVO AND INVITRO
TOXIC DNA DAMAGE BY HYDROGEN-PEROXIDE THROUGH THE FENTON REACTION INVIVO AND INVITRO
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DOI：
10.1126/science.2834821
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发表时间：
1988-04-29
期刊：
影响因子：
56.9
通讯作者：
LINN, S
中科院分区：
文献类型：
--
作者：
IMLAY, JA;CHIN, SM;LINN, S
大肠杆菌暴露于低浓度的过氧化氢会导致DNA损伤，导致诱变并杀死细菌，而较高浓度的过氧化物会减少这种损伤的量。早期的研究表明，DNA直接氧化剂是过氧化氢的衍生物，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铁物质的可用性，它们一起介导芬顿反应，其中亚铁将过氧化氢还原为反应性自由基。建立了一种体外芬顿体系，该体系产生DNA链断裂并使噬菌体失活，并且还再现了高浓度过氧化物对DNA损伤的抑制。直接DNA氧化剂在体内和在该体外系统中表现出与自由羟基自由基不同的反应性，并且可以替代为铁基自由基。
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 and in this in vitro system exhibits reactivity unlike that of a free hydroxyl radical and may instead be a ferryl radical.