[Oxidative stress in multiple sclerosis]

Abstract

Accumulating data indicate that oxidative stress (OS) plays a major role in the pathogenesis of multiple sclerosis (MS). Reactive oxygen species (ROS), leading to OS, generated in excess primarily by macrophages, have been implicated as mediators of demyelization and axonal damage in MS. ROS cause damage to main cellular components such as lipids, proteins and nucleic acids (e.g., RNA, DNA), resulting in cell death by necrosis or apoptosis. In addition, weakened cellular antioxidant defense systems in the central nervous system (CNS) in MS, and its vulnerability to ROS effects may augmented damage. Thus, treatment with antioxidants might theoretically prevent propagation of tissue damage and improve both survival and neurological outcome. Central nervous system is particularly susceptible to ROS-induced damage due to the high oxygen demands of the brain and low concentration of endogenous antioxidants. Its refer both enzymatic antioxidants: catalase, glutathione peroxidase, glutathione reductase, superoxide dismutase and nonenzymatic antioxidants glutathione, vitamins A,C,D, coenzym Q, uric acid etc. Enzymatic and non enzymatic antioxidants like vitamins, micro and macro elements could regulate progress and function different immunologic cells. Modulation of immunologic processes by this components could be an effective method in decreased risk of incidence of disease and(or) treatment of MS or other immunologic diseases.