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The overloading of body iron plays a role as an oxidative stressor

active radicals can affect lipids, proteins, and deoxyribonucleic acid (DNA), resulting in tissue injury and dysfunction

Excess iron causes oxidative stress and induces inflammation, leading to renal disease progression

iron and ascorbate has long been used as an oxidizing system; the combination of these two reagents is referred to as the Udenfriend system

ascorbate serves as a reducing cofactor for many enzymes

uptake of ascorbate from the intestinal tract is very tightly controlled

Inflammation is the most predominant feature during the early (relaping) phases of the disease and declines with aging of the patients and disease duration

anti-inflammatory or immunomodulatory treatments are effective in the relapsing stage, but the benefit is lost when the patients have entered the progressive phase

in the process of oligodendrocyte destruction and demyelination in MS lesions iron is liberated from its intracellular ferritin bound stores into the extracellular space, where it is taken up by microglia and macrophages and again stored together with ferritin. When this happens in MS lesions in an environment, where free radicals are produced by oxidative burst, iron can be liberated from ferritin and transformed into reactive Fe++[114], which reacts with hydrogen peroxide to generate highly reactive hydroxyl radicals [36] and thus amplifies oxidative damage and associated cellular injury