Multiple sclerosis and oxidative stress—a clinical perspective

Multiple Sclerosis (MS) has been traditionally considered to be a chronic inflammatory disease of central nervous system (CNS), resulting in demyelization and clinical presentation of physical disability. Such understanding of MS was solely related to neuroinflammation and its harmful effects; however, count-less data suggest the importance of neurodegenerative mechanisms that are evident in chronic demyelization plaques, and believed to be initiated by oxidative stress. CNS is particularly sensitive to oxidative attack due to the high level of oxygen utilization, relatively small amounts of conventional antioxidants and antioxidative enzymes, and large amounts of polyunsaturated lipids, biomolecules highly susceptible to oxidation. The role and significance of reactive oxygen species (ROS) in MS development has not been fully understood yet, it is believed that ROS formation is primarily orchestrated by immunoinflammatory mechanisms, but there are also data suggesting that certain inflammation independent mechanisms can result in neuronal degeneration and demyelization. They are mainly related to abnormal mitochondria functioning, glutamate excitotoxicity and the disruption of redox active metal homeostasis. Today, there is still a debate whether MS is an immunoinflammatory or neurodegenerative disorder; is it a cause or a consequence of oxidative stress, although clinical trials show encouraging results of antioxidant therapy usage in the disease management.