Imlay J A, Linn S
University of California, Berkeley.
Science. 1988 Jun 3;240(4857):1302-9. doi: 10.1126/science.3287616.
A major portion of the toxicity of hydrogen peroxide in Escherichia coli is attributed to DNA damage mediated by a Fenton reaction that generates active forms of hydroxyl radicals from hydrogen peroxide, DNA-bound iron, and a constant source of reducing equivalents. Kinetic peculiarities of DNA damage production by hydrogen peroxide in vivo can be reproduced by including DNA in an in vitro Fenton reaction system in which iron catalyzes the univalent reduction of hydrogen peroxide by the reduced form of nicotinamide adenine dinucleotide (NADH). To minimize the toxicity of oxygen radicals, the cell utilizes scavengers of these radicals and DNA repair enzymes. On the basis of observations with the model system, it is proposed that the cell may also decrease such toxicity by diminishing available NAD(P)H and by utilizing oxygen itself to scavenge active free radicals into superoxide, which is then destroyed by superoxide dismutase.
过氧化氢对大肠杆菌的毒性主要归因于由芬顿反应介导的DNA损伤，该反应从过氧化氢、与DNA结合的铁以及持续的还原当量来源中产生活性形式的羟基自由基。通过将DNA纳入体外芬顿反应系统，可以再现体内过氧化氢产生DNA损伤的动力学特性，在该系统中，铁催化烟酰胺腺嘌呤二核苷酸（NADH）的还原形式对过氧化氢的单价还原反应。为了将氧自由基的毒性降至最低，细胞会利用这些自由基的清除剂和DNA修复酶。基于对模型系统的观察，有人提出细胞也可能通过减少可用的NAD(P)H以及利用氧气本身将活性自由基清除为超氧化物来降低这种毒性，然后超氧化物会被超氧化物歧化酶破坏。
