Author(s)

Hiba A. Awooda^1,2

¹College of Applied Sciences, AlMaarefa University, Riyadh, Saudi Arabia.
²Faculty of Medicine, Al Neelain University, Khartoum, Sudan.

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.

Reactive Oxygen Species, Reactive Nitrogen Species, Cerebral Ischemia, Oxidative Stress

Awooda, H. (2019) Pathophysiology of Cerebral Ischemia: Role of Oxidative/Nitrosative Stress. Journal of Biosciences and Medicines, 7, 20-28. doi: 10.4236/jbm.2019.73003.