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Oxidative stress in the chronic phase after stroke.
Margarita L Alexandrova1, Petyo G Bochev, Vanya I Markova
1Department of Biophysics, Medical University, Pleven, Bulgaria. margalexandrova@hotmail.com
Redox Report : Communications in Free Radical Research
|August 26, 2003
Summary
Patients with chronic stroke show increased spontaneous reactive oxygen species (ROS) generation by phagocytes and elevated oxidative damage to lipids. Managing free radicals may prevent further vascular injury and recurrent strokes.
Area of Science:
- Neuroscience
- Immunology
- Biochemistry
Background:
- Stroke, both ischemic and hemorrhagic, leads to chronic vascular injury.
- Oxidative stress plays a significant role in the pathophysiology of stroke.
- Understanding the long-term effects of stroke on oxidative processes is crucial for developing effective treatments.
Purpose of the Study:
- To evaluate spontaneous and stimulated reactive oxygen species (ROS) generation by phagocytes in chronic stroke patients.
- To assess blood antioxidant capacity and oxidative damage markers in these patients.
- To investigate the relationship between stroke type, time post-stroke, and oxidative stress markers.
Main Methods:
- Peripheral blood phagocytes were analyzed for spontaneous and stimulated extracellular ROS generation.
- Blood antioxidant capacity was measured.
- Levels of plasma lipid peroxides and thiobarbituric acid-reactive material were quantified.
- Patients in the chronic phase of severe ischemic and hemorrhagic stroke were compared to a control group.
Main Results:
- Enhanced spontaneous phagocyte oxidative activity was observed in stroke patients, irrespective of stroke type or time elapsed.
- No significant differences were found in stimulated ROS generation or blood antioxidant capacity.
- Elevated concentrations of plasma lipid peroxides and thiobarbituric acid-reactive material were detected in stroke patients, with lipid peroxides increasing over time.
Conclusions:
- Patients in the chronic phase of stroke exhibit heightened spontaneous phagocyte oxidative activity and increased oxidative lipid damage.
- Reducing circulating ROS and lipid peroxidation products may mitigate chronic vascular injury and reduce the risk of secondary stroke.
- Complex therapeutic strategies, including antioxidant treatments, are recommended to manage post-stroke oxidative stress.