Pathophysiology of Cerebral Ischemia: Role of Oxidative/Nitrosative Stress

Abstract

Stroke is a devastating disease with a complex pathophysiology; it ranks second to ischemic heart disease as a cause of death and long-term disability. Tissue damage results from diverse mechanisms with central involvement of free radicals’ overproduction that results in oxidative stress and hence contributes to brain damage. Free radicals [Reactive oxygen species/Reactive nitrogen species] play central a role in the diverse normal physiological processes and as defense mechanisms against harmful substances. When the rate of their production exceeds the anti-oxidant capacity of the body, oxidative stress occurs. Oxidative stress is implicated in the pathogenesis of various diseases including hypertension, atherosclerosis, diabetes mellitus and cancer; they mediate damage to cell structures, lipid peroxidation, protein denaturation, nucleic acid and DNA damage.