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Superoxide, superoxide dismutase and ischemic injury
Daniela Salvemini1, Salvatore Cuzzocrea
1MetaPhore Pharmaceuticals Inc, St Louis, MO 63114, USA. dsalvemini@metaphore.com
Current Opinion in Investigational Drugs (London, England : 2000)
|July 26, 2002
Summary
Oxidative stress from excess oxidants contributes to ischemia-reperfusion injury. Superoxide dismutase mimetics (SODm) show promise in preventing this cellular damage and improving outcomes.
Area of Science:
- Biochemistry
- Cellular Biology
- Pathophysiology
Background:
- Oxidative stress, an imbalance between oxidants and antioxidants, is increasingly implicated in ischemia and reperfusion (I/R) injury.
- Reactive oxygen species (ROS), particularly superoxide and peroxynitrite, are key mediators of endothelial and tissue damage during I/R events.
Purpose of the Study:
- To review the significant role of superoxide and peroxynitrite in I/R-induced cellular injury.
- To discuss the therapeutic potential of superoxide dismutase mimetics (SODm) in mitigating I/R damage.
Main Methods:
- Review of immunohistochemical and biochemical evidence.
- Analysis of molecular mechanisms of oxidative damage in I/R.
- Evaluation of in vivo studies on SODm efficacy.
Main Results:
- Superoxide and peroxynitrite contribute to endothelial damage, neutrophil infiltration, lipid peroxidation, and mitochondrial dysfunction.
- Oxidative stress activates pathways like poly-ADP ribosyl synthetase, exacerbating cellular injury.
- SODm effectively prevent energetic failure and tissue damage in I/R models.
Conclusions:
- Superoxide and peroxynitrite are critical contributors to I/R pathophysiology.
- Superoxide dismutase mimetics represent a promising therapeutic strategy for I/R injury.