Suplementação com vitaminas, um fator complicador ou benéfico para portadores ou não de Alzheimer durante o processo de envelhecimento?

Abstract

Aging is an experience every human being shares, but not always understands. The nature of aging process has been target for numerous speculations. Suggested possibilities include: change in the DNA code, reduction of protein synthesis, macromolecules links, auto-attack to immune system and damage caused by oxidative reactions. Evidences accumulated indicate that aging and diseases related to aging are caused primarily due to damage generated by free radicals. An example of one of these diseases is Alzheimer, the most prevalent form of dementia, with cognitive loss that occurs during aging. It is a disease that alters behavior, memory, learning, daily activities and life quality. Oxidative stress occurs before the establishment of pathological plaques in Alzheimer. The accumulation of reactive species by exogenous and endogenous production is called oxidative stress being common in many kinds of cells with reduced redox power. The mononuclear cells, as lymphocytes and monocytes are pre cells that generate free radical as do themselves. Oxidative stress is an imbalance between free radical and antioxidant defense. Antioxidants are responsible for inhibition and reduction of lesions caused by free radicals in cells. Examples of these nutrients are vitamins C, E and beta-carotene. In a mutant science of few conclusive results, investigations continue about the benefits, or maybe downside of antioxidants not only for sick people, but giving special attention to the highest consumers, the healthy population. So, our objective was to evaluate the possible dual effect (antioxidant and prooxidant) of the vitamin complex (ascorbic acid, alpha-tocopherol and beta-carotene) in mononuclear cells and plasma of non Alzheimer and Alzheimer patients during the aging process. Mononuclear cells and plasma were obtained from peripheral blood and incubated with the following concentrations of the vitamin complex: [A] Ascorbic acid = 2,82µg, Alpha-tocopherol = 3,45µg, Beta-Carotene =0,09µg;[B] Ascorbic acid = 5,64µg, Alpha-tocopherol = 6,90µg, Beta-Carotene =0,18µg; [C] Ascorbic acid = 14,09µg, Alpha-tocopherol = 17,23µg, Beta-Carotene =0,43µg; [D] Ascorbic acid = 28,18µg, Alpha-tocopherol = 34,46µg, Beta-Carotene =0,86µg. Two assays were done: chemioluminescence to evaluate the oxidative compartment and MTT to evaluate the reductive compartment in cells and plasma. Albumin and uric acid were also measured by kit LabTest. Our results demonstrated that non Alzheimer donors Don not have the cellular benefit of supplementation with the vitamins studied and that there may be a plasmatic compensation of the cellular effects. The recommended dos is ideal, as food, to guarantee an antioxidant effect and not pro-oxidant as shown. We concluded that different age groups need different quantities of vitamins and that high doses can be evil to elderly individuals. Alzheimer patients benefited in all compartments with all vitamin doses of the complex. We conclude that a higher vitamin ingestion for this group, as food, is recommended to balance the oxidative and reductive compartments.