Harris E D, Percival S S
Department of Biochemistry and Biophysics, Texas A&M University, College Station 77843-2128.
Am J Clin Nutr. 1991 Dec;54(6 Suppl):1193S-1197S. doi: 10.1093/ajcn/54.6.1193s.
Scurvy-like symptoms have been seen in experimental copper deficiency. This forecasts a role for the vitamin in copper metabolism. Ascorbate has been known to antagonize the intestinal absorption of copper. More recent studies have characterized a postabsorption role for ascorbate in the transfer of copper ions into cells. The vitamin reacts directly or indirectly with ceruloplasmin, a serum copper protein, specifically labilizing the bound copper atoms and facilitating their cross-membrane transport. Ascorbate at physiological levels and above impedes the intracellular binding of copper to Cu,Zn superoxide dismutase. The mechanism is unclear but nonetheless suggests both positive and negative regulatory functions for ascorbate in copper metabolism.
在实验性铜缺乏症中已观察到类似坏血病的症状。这预示着该维生素在铜代谢中发挥作用。已知抗坏血酸会拮抗肠道对铜的吸收。最近的研究已明确抗坏血酸在铜离子转运到细胞过程中的吸收后作用。该维生素直接或间接与铜蓝蛋白（一种血清铜蛋白）发生反应，特异性地使结合的铜原子不稳定，并促进其跨膜运输。生理水平及以上的抗坏血酸会阻碍铜在细胞内与铜锌超氧化物歧化酶的结合。其机制尚不清楚，但这仍表明抗坏血酸在铜代谢中具有正负调节功能。
