Functions of vitamin C as a mediator of transmembrane electron transport in blood cells and related cell culture models.

H Goldenberg, H Landertshamer, H Laggner

Index: Antioxid. Redox Signal. 2 , 189-196, (2000)

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Abstract

Vitamin C (ascorbic acid) is an important physiological antioxidant. Within cells, it is practically always present in the reduced form. Several enzymatic and nonenzymatic mechanisms have been reported to maintain this status. In the extracellular environment, oxidation of ascorbate leads to loss of vitamin because the oxidized form, dehydroascorbic acid, is unstable under physiological conditions. The intermediate ascorbate free radical, although rather long-lived for a free radical, quickly disproportionates into the two other forms, also leading to loss of vitamin. Protection from loss can only be achieved by cellular regeneration mechanisms, i.e., by uptake of dehydroascorbic acid and either storage or recycling, and by plasma-membrane mediated reduction of extracellular free radical or dehydroascorbic acid. Moreover, intracellular ascorbate can also serve as an electron donor for transmembrane reduction of external electron acceptors. However, the physiological significance of this function is as yet unknown. The results presented in the literature are sometimes conflicting as to the relative contributions of these different possibilities, which seem to differ in different cell types. In this short review, the various pathways of regeneration of ascorbate and their relative contributions to the avoidance of vitamin loss in plasma or cell culture medium are discussed.