Prabhu H R, Krishnamurthy S
Department of Biochemistry, Kasturba Medical College, Mangalore.
Indian J Biochem Biophys. 1993 Oct;30(5):289-92.
The autoxidation of L-ascorbate on incubation in saline phosphate buffer (pH 7.4) is accompanied by hydroxyl radical (.OH) generation. The metal chelator EDTA showed significant inhibition of ascorbate autoxidation and ascorbate-dependent .OH release. On the other hand, Fe2+ (EDTA) greatly augmented both ascorbate autoxidation and ascorbate-dependent .OH production. The biological iron chelating compounds such as ATP, ADP, citrate and pyrophosphate suppressed both ascorbate autoxidation and ascorbate-mediated .OH production, thereby indicating that these compounds suppress the activating effect of iron. Ascorbate autoxidation and ascorbate-dependent .OH formation, stimulated by Fe2+ (EDTA) were significantly inhibited by .OH scavengers, namely mannitol, thiourea and sodium formate, as well as by catalase and to a lesser extent by bovine serum albumin, superoxide dismutase (native and heat denatured) and heat denatured catalase.
L-抗坏血酸盐在磷酸盐缓冲液（pH 7.4）中孵育时的自氧化过程伴有羟基自由基（·OH）的产生。金属螯合剂EDTA对抗坏血酸盐的自氧化以及抗坏血酸盐依赖性·OH的释放具有显著的抑制作用。另一方面，Fe2+（EDTA）极大地增强了抗坏血酸盐的自氧化以及抗坏血酸盐依赖性·OH的产生。生物铁螯合化合物如ATP、ADP、柠檬酸盐和焦磷酸盐，既抑制了抗坏血酸盐的自氧化，也抑制了抗坏血酸盐介导的·OH的产生，从而表明这些化合物抑制了铁的激活作用。由Fe2+（EDTA）刺激产生的抗坏血酸盐自氧化和抗坏血酸盐依赖性·OH的形成，受到·OH清除剂（即甘露醇、硫脲和甲酸钠）以及过氧化氢酶的显著抑制，牛血清白蛋白、超氧化物歧化酶（天然型和热变性型）以及热变性过氧化氢酶也有一定程度的抑制作用。
