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.
Highlights
Stroke is the second leading cause of death and the third leading reason of permanent disability in adults worldwide [1] [2]
All cells use oxygen to produce energy; free radicals are formed as a result of adenosine triphosphate (ATP) production by the mitochondria and known as reactive oxygen species (ROS)
Free radical production is increased in ischemic and hemorrhagic stroke, leading to oxidative stress that contributes to brain damage
Summary
Stroke is the second leading cause of death and the third leading reason of permanent disability in adults worldwide [1] [2]. According to the World Health Organization (WHO), stroke has globally affected a total of 15 million people each year. The WHO describes a stroke as an interruption to the supply of blood to the brain, with “rapidly developing clinical signs of focal or global disruption of cerebral function, with signs lasting 24 hours or longer, or leading to death with no apparent cause other than vascular origin”. There are two major mechanisms causing brain damage in stroke patients: Hemorrhage and Ischemia which represents about 70% to 80% of all strokes’ cases. Recent researches have suggested link between an excessive generation of reactive oxygen species [ROS] and the development of neuronal death in acute brain injury like brain trauma and cerebral ischemia [9]. Excessive ROS generation can induce the functional and structural damage of neuronal cells and may play an important role in the pathophysiology of cerebral ischemia [10] [11]
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