Grieger M, Schulz S
Folia Haematol Int Mag Klin Morphol Blutforsch. 1983;110(3):427-36.
Determining SOD in red blood cells was made in 26 carriers of G6PD defect 9 haemicygotic mark carriers and 16 heterocytic mark carriers had a diminished SOD enzyme activity. This is probably due to an inactivation of SOD by diminished reductive equivalents in the metabolism of defect cells. In this way, more oxidatively effective radicals will appear, even OH. among them. The latter may render the enzyme ineffective by binding it to the imidazol group in the catabolic centre. Consequently, an accumulation of the substrate O2-. may lead to a further cell damage, thus causing an increased haemolysis.
对26名葡萄糖-6-磷酸脱氢酶(G6PD)缺陷携带者的红细胞进行超氧化物歧化酶(SOD)检测,其中9名半合子标记携带者和16名杂合子标记携带者的SOD酶活性降低。这可能是由于缺陷细胞代谢中还原当量减少导致SOD失活。这样一来,会出现更多氧化活性更强的自由基,其中甚至包括羟基自由基(OH)。后者可能通过与分解代谢中心的咪唑基团结合而使该酶失去活性。因此,底物超氧阴离子(O2-)的积累可能导致细胞进一步受损,从而引起溶血增加。