Brief Overview about Oxidative stress in Multiple Sclerosis

Abstract

Multiple sclerosis (MS) is an inflammatory and neurodegenerative disorder of the central nervous system (CNS), characterized by immune-mediated damage to cells in the white and gray matter of the brain, spinal cord, and optic nerve through demyelination and axonal degeneration. Oxidative stress is an imbalance between oxidants and anti- oxidants infavor of the oxidants, leading to a disruption of redox (oxidation reduction) signaling and control and or molecular damage. The ROS are reactive species derived from oxygen that include the superoxide anion (O-), hydrogen peroxide (H2O2), and the hydroxyl radical (OH). The RNS are reactive species derived from nitrogen and include nitric oxide (NO∙) and peroxynitrite (ONOO-). The ROS and RNS are extremely unstable and reactive because they have an unpaired electron in their outer orbital. They take electrons from proteins, lipids, carbohydrates, and nucleic acids, causing damage to biological membranes, genetic material, and other macromolecules. Oxidative stress is induced by externally added oxidants and compounds either stimulating ROS production or weakening antioxidant defense. The development of neurodegeneration in MS is a complex process that may be related to primary apoptosis, synaptopathy, and excitotoxicity associated with glutamate overload, ionic channel dysfunction, calcium overload, mitochondriopathy, proteolytic enzyme production, and activation of apoptotic pathways. It is also important that mitochondrial dysfunction results in an increased production of reactive oxygen species (ROS), which is detrimental to neurons and glia. On the other hand, OS damages the mitochondria, which disrupts the transport of adenosine triphosphate along the axon, and consequently leads to neurodegeneration.