Benov Ludmil, Fridovich Irwin
Department of Biochemistry, Faculty of Medicine, Kuwait University, P.O. Box 24923, Safat, Kuwait.
Arch Biochem Biophys. 2002 Nov 1;407(1):45-8. doi: 10.1016/s0003-9861(02)00498-8.
The ability of short-chain sugars to cause oxidative stress has been examined using glycolaldehyde as the simplest sugar. Short-chain sugars autoxidize in air, producing superoxide and alpha,beta-dicarbonyls. In Escherichia coli the soxRS regulon mediates an oxidative stress response, which protects the cell against both superoxide-generating agents and nitric oxide. In superoxide dismutase-deficient E. coli mutants, glycolaldehyde induces fumarase C and nitroreductase A, which are regulated as members of the soxRS regulon. A mutational defect in soxRS eliminates that induction. This establishes that glycolaldehyde can cause induction of this defensive regulon. This effect of glycolaldehyde was oxygen-dependent, was not shown by glyoxal, and was not seen in the superoxide dismutase-replete parental strain, and it was abolished by a cell-permeable SOD mimetic. All of these suggest that superoxide radicals produced by the oxidation of glycolaldehyde played a key role in the induction.
已使用乙醇醛作为最简单的糖类来研究短链糖类引发氧化应激的能力。短链糖类在空气中自动氧化,产生超氧化物和α,β - 二羰基化合物。在大肠杆菌中,soxRS调节子介导氧化应激反应,保护细胞免受超氧化物生成剂和一氧化氮的侵害。在超氧化物歧化酶缺陷型大肠杆菌突变体中,乙醇醛诱导延胡索酸酶C和硝基还原酶A,它们作为soxRS调节子的成员受到调控。soxRS中的突变缺陷消除了这种诱导作用。这表明乙醇醛可导致这种防御性调节子的诱导。乙醇醛的这种作用依赖于氧气,乙二醛未表现出该作用,在超氧化物歧化酶充足的亲本菌株中也未观察到,并且它被一种细胞可渗透的超氧化物歧化酶模拟物所消除。所有这些表明,乙醇醛氧化产生的超氧自由基在诱导过程中起关键作用。