Benov Ludmil, Beema Anees F, Sequeira Fatima
Department of Biochemistry, Faculty of Medicine, Kuwait University, PO Box 24923 Safat, 13110, Kuwait.
Biochim Biophys Acta. 2003 Jul 23;1622(2):128-32. doi: 10.1016/s0304-4165(03)00134-x.
Increase in the production of triosephosphates has been considered an important factor leading to diabetic complications. It might be expected that like the other short chain monosaccharides, triosephosphates autoxidize producing superoxide radical and alpha,beta-diketones. Since superoxide can also initiate the oxidation of short chain sugars, free radical chain reactions are possible. If such reactions occur in vivo, triosephosphates would be more deleterious to cells lacking superoxide dismutase (SOD) than to normal cells. Here we demonstrate that triosephosphates kill a SOD-deficient Escherichia coli mutant much more than the parental, SOD-proficient strain. The effect is oxygen-dependent and is partially suppressed by aminoguanidine. Increased production of superoxide and diketones appeared to be the cause of triosephosphates toxicity.
磷酸丙糖产量的增加被认为是导致糖尿病并发症的一个重要因素。可以预期，与其他短链单糖一样，磷酸丙糖会自动氧化产生超氧自由基和α,β - 二酮。由于超氧也能引发短链糖的氧化，自由基链式反应是可能的。如果这种反应在体内发生，磷酸丙糖对缺乏超氧化物歧化酶（SOD）的细胞的危害将比对正常细胞更大。在这里，我们证明磷酸丙糖对缺乏SOD的大肠杆菌突变体的杀伤作用比对亲本的、具有SOD活性的菌株大得多。这种作用依赖于氧气，并且被氨基胍部分抑制。超氧和二酮产量的增加似乎是磷酸丙糖毒性的原因。
