Padh H
Department of Biochemistry and Molecular Biology, University of Chicago, IL 60637.
Nutr Rev. 1991 Mar;49(3):65-70. doi: 10.1111/j.1753-4887.1991.tb07407.x.
Ever since the discovery of vitamin C (ascorbic acid), scientists have been intrigued as to how ascorbic acid deficiency can lead to the diverse symptoms exhibited in scurvy. Only in recent years has it been appreciated that ascorbic acid has important functions in many cellular reactions and processes in addition to its role in collagen synthesis. The few such reactions that are understood at the molecular level make it apparent that ascorbic acid does not directly participate in enzyme-catalyzed conversion of substrate to product. Instead, the vitamin regenerates prosthetic metal ions in these enzymes in their required reduced forms. This is in agreement with other antioxidant functions of vitamin C, e.g., scavenging of free radicals. Ascorbate and other antioxidant nutrients are presumed to play a pivotal role in minimizing the damage from oxidative products, including free radicals. This protective function is twofold: the already-oxidized groups in prosthetic centers of enzymes are reduced and the oxidants and free radicals are removed.
自从发现维生素C（抗坏血酸）以来，科学家们一直对抗坏血酸缺乏如何导致坏血病中出现的多种症状感到好奇。直到最近几年，人们才认识到抗坏血酸除了在胶原蛋白合成中发挥作用外，在许多细胞反应和过程中也具有重要功能。在分子水平上理解的少数此类反应表明，抗坏血酸并不直接参与酶催化的底物到产物的转化。相反，这种维生素能将这些酶中的辅助金属离子再生为所需的还原形式。这与维生素C的其他抗氧化功能一致，例如清除自由基。抗坏血酸盐和其他抗氧化营养素被认为在将包括自由基在内的氧化产物的损害降至最低方面起着关键作用。这种保护功能有两个方面：酶的辅助中心中已经氧化的基团被还原，氧化剂和自由基被清除。
