Reactive oxygen species and ischemic cerebrovascular disease

Inan Olmez, Huseyin Ozyurt

Research output: Contribution to journalShort surveypeer-review

170 Scopus citations

Abstract

Stroke is an emerging major health problem often resulting in death or disability. Hyperlipidemia, high blood pressure and diabetes are well established risk factors. Endothelial dysfunction associated with these risk factors underlies pathological processes leading to atherogenesis and cerebral ischemic injury. While mechanisms of disease are complex, endothelial dysfunction involves decreased nitric oxide (NO) and elevated levels of reactive oxygen species (ROS). At physiological levels, ROS participate in regulation of cellular metabolism. However, when ROS increase to toxic levels through imbalance of production and neutralization by antioxidant enzymes, they cause cellular injury in the form of lipid peroxidation, protein oxidation and DNA damage. Central nervous system cells are more vulnerable to ROS toxicity due to their inherent higher oxidative metabolism and less antioxidant enzymes, as well as higher content of membranous fatty acids. During ischemic stroke, ROS concentration rises from normal low levels to a peak point during reperfusion possibly underlying apoptosis or cellular necrosis. Clinical trials and animal studies have shown that natural compounds can reduce oxidative stress due to excessive ROS through their antioxidant properties. With further study, we may be able to incorporate these compounds into clinical use with potential efficacy for both the treatment and prevention of stroke.

Original languageEnglish (US)
Pages (from-to)208-212
Number of pages5
JournalNeurochemistry International
Volume60
Issue number2
DOIs
StatePublished - Jan 2012

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience
  • Cell Biology

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