The role of free radicals and oxidative damage in relation to cellular aging is a subject that has received considerable attention recently. It has been well documented that in vivo free radicals are highly reactive with polyunsaturated phospholipids of membranes, nucleic acids, proteins, and polysaccharides. When radicals react with these components, the result is extensive damage to chemical bonds and membranes leading to polymerisation, accumulation of debris, loss of membrane and enzymatic integrity, and cell death. Free radicals are formed endogenously during normal cellular metabolism and metabolism of certain drugs and other foreign substances. Exogenously, free radicals are generated during exposure to environmental pollutants, including cigarette smoke. Free radical and oxidative damage that accumulate as we age may contribute to the diseases associated with ageing. Previous studies have indicated that vitamin E (α-tocopherol) can protect the cell from free radical damage. It was shown that vitamin E deficiency leading to increased oxidation causes premature ageing of band 3. Band 3, the anion transport protein, is the most heavily used ion transport system in vertebrates and is a ubiquitous family of proteins. It is present in all cells and tissues examined including brain and lymphocytes. Not only is band 3 present in cell membranes, but also in nuclear, Golgi, and mitochondrial membranes. Band 3 is involved in respiration and acid-base balance, and is the major structural protein linking the plasma membrane to the cytoskeleton. Oxidation generates senescent cell antigen (SCA). An ageing antigen, that is a protein that appears on old cells and acts as a specific signal for the termination of that cell by initiating the binding of IgG autoantibody and subsequent removal by phagocytes.
Results of the scientific studies indicate that anion transport by lymphocytes declines with age and that this decline can be delayed or prevented by increased levels of vitamin E in the diet. Vitamin E delayed band 3 ageing/posttranslational modifications as determined by binding of aged/altered band 3 antibodies and anion transport. This may be a mechanism by which vitamin E supplements lessen the effects of ageing. β-carotene did not alter the effect of age on anion transport or binding to aged/altered brain band 3. However, vitamin E acts at the membranes where transport proteins reside, whereas β-carotene may not. Thus, β-carotene may have other effects that would not be detected in this study. No evidence for in vivo synergy between vitamin E and β-carotene was found.
Fig 1. Effect of antioxidant treatment on binding of aged band 3 antibodies (980) to mouse brain membranes. Data are presented as mean number of antibody molecules per pg membrane protein 6 SE.
It appears that vitamin E can reduce oxidative damage occurring during ageing in at least two of the crucial systems, the immune and central nervous system. Band 3 represents a major ''communication'' protein because anion transport is required for most, if not all, cellular processes and cellular responses, and band 3 is present in intracellular organelles including mitochondria, Golgi, nuclear, and cellular membranes. Alteration in band 3 would affect all networks. Further investigations should determine whether vitamin E prolongs life span.