Biochemical mechanism of oxidative damage by redox-cycling drugs.
Biochemical mechanism of oxidative damage by redox-cycling drugs.
复制标题
氧化还原循环药物氧化损伤的生化机制。
DOI：
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发表时间：
1985
影响因子：
10.4
通讯作者：
M. Ciriolo
中科院分区：
文献类型：
--
作者：
Giuseppe Rotilio;Irene Mavelli;Luisa Rossi;M. Ciriolo
氧化还原循环药物的氧化还原中间体产生的生化机制包括：光化学事件，光电离过程或光激发态的电子转移;药物的还原形式与氧结合血红素蛋白的氧态的电子交换;催化金属中心的氧化（氧化酶、过氧化物酶、加氧酶）;或电子从活化的细胞内电子转移链（线粒体、微粒体等）转移到药物的氧化形式。这些药物自由基的进一步反应可以通过直接攻击生物大分子或通过氧还原产生O2-、H2 O2和OH而导致氧化损伤。反应途径取决于金属离子、天然清除剂、控制活性物质相对浓度的酶以及环境中氧气的可用性。
Biochemical mechanisms of production of redox intermediates of redox-cycling drugs include: photochemical events, either photoionization process or electron transfer from photoexcited states; electron exchange of reduced form of a drug with the oxy state of oxygen-binding hemoproteins; oxidation by catalytic metal centers (oxidases, peroxidases, oxygenases) of the reduced forms of drugs; or electron transfer to the oxidized form of a drug from activated intracellular electron transfer chain (mitochondria, microsomes, etc.). Further reaction of these drug free radicals can lead to oxidative damage by either direct attack of biological macromolecules or via oxygen reduction, giving O2-, H2O2, and OH. The reaction pathway depends on the presence of metal ions, natural scavengers, enzymes that control relative concentrations of reactive species, and availability of oxygen in the environment.
影响因子：
2.9
作者：
MARSHALL, LE;GRAHAM, DR;SIGMAN, DS
通讯作者：
SIGMAN, DS