Benov L
Department of Biochemistry, Faculty of Medicine, Kuwait University, P.O. Box 24923, Safat 13110, Kuwait.
Protoplasma. 2001;217(1-3):33-6. doi: 10.1007/BF01289410.
Superoxide is considered to be poorly reactive, and cell damage has been attributed to HO. generated via the Haber-Weiss reaction. The function of O2- in this reaction is only to reduce Fe3+ to Fe2+. In vivo, however, superoxide could not out-compete cellular reductants such as glutathione, NADPH, and ascorbate, which makes the observed O2- toxicity rather puzzling. Little attention has been paid to the idea that, irrespective of its poor chemical reactivity, superoxide might be capable of interacting directly with specific intracellular targets; and that even the Haber-Weiss reaction might be a consequence of such direct interactions. This paper summarizes latest data that support the concept of such a mechanism.
超氧化物被认为反应活性较低,细胞损伤归因于通过哈伯-维希反应产生的羟基自由基(HO·)。超氧阴离子(O₂⁻)在该反应中的作用仅是将Fe³⁺还原为Fe²⁺。然而,在体内,超氧化物无法与细胞内的还原剂如谷胱甘肽、NADPH和抗坏血酸竞争,这使得所观察到的超氧阴离子毒性相当令人费解。很少有人关注这样一种观点,即尽管超氧化物的化学反应活性较低,但它可能能够直接与特定的细胞内靶点相互作用;甚至哈伯-维希反应可能是这种直接相互作用的结果。本文总结了支持这种机制概念的最新数据。