Free radical-mediated peroxidation of biological molecules, especially of lipids, is implicated in the pathogenesis of a number of diseases like multiple sclerosis. Low concentration of antioxidant vitamins: beta carotene, retinol, alpha tocopherol and ascorbic acid have been observed in serum or cerebrospinal fluid of multiple sclerosis patients. On the basis of these observations, we studied the potential lipoprotein oxidation and total antioxidant capacity in the pathogenesis of multiple sclerosis. Lipoprotein oxidizability for plasma in vitro, serum levels of autoantibodies against oxidized low-density lipoproteins, plasma total homocysteine levels with vitamin B12 and folate, and plasma total antioxidant capacity were measured in twenty four patients with multiple sclerosis and twenty four healthy sex- and age-matched person as control. In multiple sclerosis patients during an attack, a significant increase in both in vitro lipid oxidizability for plasma and in the levels of autoantibodies against oxidized low-density lipoproteins, and a strong decrease in plasma total antioxidant capacity were detected. Plasma total homocysteine levels were significantly higher in multiple sclerosis patients whose plasma vitamin B12 and folate levels were lower but not statistically significant, than controls. The present study indicates that lipoprotein oxidation may be important factor in the course of multiple sclerosis and in vitro measurements of plasma oxidation kinetics as an indication for lipoprotein oxidation might be useful as an additional tool for the clinical diagnosis of multiple sclerosis.

We determined serum levels of ascorbic acid, betacarotene, retinol and alpha tocopherol and lipid peroxidation (as estimated by thiobarbituric acid reacting substances (TBARS) generation) in 24 multiple sclerosis (MS) patients and 24 healthy sex- and age-matched person as control. The levels of four antioxidant vitamins were significantly lower in MS patients compared to controls (p < 0.05). TBARS levels were significantly higher in the patients of MS compared to the controls (p = 0.001). In MS patients, the levels of beta-carotene, alpha tocopherol and ascorbic acid correlated significantly with each other (r2 = 0.689 - 0.779). It appeared that there was inverse correlation between the serum levels of ascorbic acid or beta-carotene, but not of alpha tocopherol or retinol, and TBARS levels in MS. The present study indicates that antioxidant vitamins (alpha tocopherol, beta-carotene, retinol and ascorbic acid) are decreased in sera of MS patients during an attack, and that this decrease may well be dependent on the increased oxidative burden as reflected by lipid peroxidation products. The role of antioxidant vitamin supplementation in prevention and/or treatment of MS remains to be explored.

In this study discussed the primary and regulatory roles of fatty acids, and investigated the affects of fatty acids on metabolic programming. Review of the literature was carried out on three electronic databases to assess the roles of fatty acids in metabolic programming. All abstracts and full-text articles were examined, and the most relevant articles were selected for screening and inclusion in this review. The mother’s nutritional environment during fetal period has important effects on long term health. Fatty acids play a primary role in growth and development. Alterations in fatty acid intake in the fetal period may increase the risk of obesity and metabolic disorders in later life. Maternal fatty acid intakes during pregnancy and lactation are passed to the fetus and the newborn via the placenta and breast milk, respectively. Imbalances in fatty acid intake during the fetal period change the fatty acid composition of membrane phospholipids, which can cause structural and functional problems in cells. Additionally, the metabolic and neuroendocrine environments of the fetus and the newborn play key roles in the regulation of energy balance. Imbalances in fatty acid intake during pregnancy and lactation may result in permanent changes in appetite control, neuroendocrine function and energy metabolism in the fetus, leading to metabolic programming. Further studies are needed to determine the role of fatty acid intake in metabolic programming.