Is ascorbic acid an antioxidant for the plasma membrane?

Abstract

Ascorbic acid, or vitamin C, is a primary antioxidant in plasma and within cells, but it can also interact with the plasma membrane by donating electrons to the alpha-tocopheroxyl radical and a trans-plasma membrane oxidoreductase activity. Ascorbate-derived reducing capacity is thus transmitted both into and across the plasma membrane. Recycling of alpha-tocopherol by ascorbate helps to protect membrane lipids from peroxidation. However, neither the mechanism nor function of the ascorbate-dependent oxidoreductase activity is known. This activity has typically been studied using extracellular ferricyanide as an electron acceptor. Whereas an NADH:ferricyanide reductase activity is evident in open membranes, ascorbate is the preferred electron donor within cells. The oxidoreductase may be a single membrane-spanning protein or may only partially span the membrane as part of a trans-membrane electron transport chain composed of a cytochrome or even hydrophobic antioxidants such as alpha-tocopherol or ubiquinol-10. Further studies are needed to elucidate the structural components, mechanism, and physiological significance of this activity. Proposed functions for the oxidoreductase include stimulation of cell growth, reduction of the ascorbate free radical outside cells, recycling of alpha-tocopherol, reduction of lipid hydroperoxides, and reduction of ferric iron prior to iron uptake by a transferrin-independent pathway.

Involvement of ROS and JNK1 in selenite-induced a poptosisin Chang liver cells

“…Ascorbate and α-tocopherol are representative antioxidant vitamins. Ascorbate acts as a major antioxidant in cytosol by donation of one-electron or hydrogen atom, and indirectly reduce the α-tocopheryl radical to α-tocopherol in cell membrane (May, 1999). α-Tocopherol acts as a scavenger of peroxyl radicals and an inhibitor of the free radical chain reaction of lipid peroxidation.…”

The increase of reactive oxygen species and their inhibition in an isolated guinea pig spinal cord compression model

“…29,37 Ascorbic acid has the potential to protect both cytosolic and membrane components of cells from oxidant damage. 38 For example, ascorbic acid scavenges free radical species in the cytosol and reduces the a-tocopheroxyl radical to a-tocopherol for cellular membranes. 38 As one of the potential treatments, hypothermia has been shown in numerous animal and clinical studies to attenuate neuronal damage and dysfunction after mechanical injury and ischemia in the spinal cord.…”

“…38 For example, ascorbic acid scavenges free radical species in the cytosol and reduces the a-tocopheroxyl radical to a-tocopherol for cellular membranes. 38 As one of the potential treatments, hypothermia has been shown in numerous animal and clinical studies to attenuate neuronal damage and dysfunction after mechanical injury and ischemia in the spinal cord. 28 The mechanisms proposed to account for the protection produced by hypothermia include reducing metabolic rate of oxygen consumption, attenuating excitotoxicity and decreasing generation of ROS.…”

Vitamin C modulation of H2O2-induced damage and iron homeostasis in human cells

“…AA is widely distributed in all tissues of the body at concentrations usually several-fold higher than in the plasma [13] and it recycles other important antioxidant molecules, such as vitamin E and glutathione [14,15]. However, the vitamin has other important, non-antioxidant biological functions [16,17], of which some are related to its ability to reduce ferric (Fe 3+ ) to ferrous (Fe 2+ ) iron.…”