Abstract
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). It is characterized by loss of myelin, the fatty tissue that surrounds and protects nerve fibres allowing them to conduct electrical impulses. Recent data indicate that oxidative stress (OS) plays a major role in the pathogenesis of multiple sclerosis (MS). The aim of this study was to estimate level of serum total antioxidative capacity in patients with multiple sclerosis. Our cross-sectional study included 33 patients with MS and 24 age and sex matched control subjects. All our patients had a Poser criteria for definite diagnostic categories of multiple sclerosis. Serum total antioxidant capacity (TAC) was measured by quantitative colorimetric determination, using Total antioxidant Capacity-QuantiCromAntioxidant Assay Kit (BioAssay systems, USA; DTAC-100). Mean serum TAC in multiple sclerosis group of patients was 119.2 mM Trolox equivalents and was significantly lower (p<0.001) compared to the control group of subjects (167.1 mM Trolox equivalents). Our results showed that oxidative stress plays an important role in pathogenesis of multiple sclerosis. This finding, also, suggests the importance of antioxidants in diet and therapy of MS patients.
Highlights
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS)
Our results showed that oxidative stress plays an important role in pathogenesis of multiple sclerosis
As macrophages produce various mediators, there are a lot of factors that could contribute to pathogenesis and development of MS [ ]
Summary
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). It is characterized by loss of myelin, the fatty tissue that surrounds and protects nerve fibres allowing them to conduct electrical impulses. Imbalanced defence mechanism of antioxidants, caused by overproduction of free radicals or their incorporation from environment to living system, leads to damage and neuro-degeneration, subsequently. Apart from several other environmental or genetic factors, oxidative stress (OS) leading to free radical attack on neural cells contributes calamitous role to neuro-degeneration. Reactive oxygen species (ROS), leading to OS, generated in excess primarily by macrophages, have been implicated as mediators of demyelization and axonal damage in both MS and experimental autoimmune encephalomyelitis (EAE), its animal model [ ]. ROS cause damage at the level of cellular components such as lipids, proteins and nucleic ac-
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