Abstract
Aim: Free radical mechanisms may play an important role in brain ischemia / reperfusion injury. The generation of reactive oxygen species by homocysteine (Hcy) or nitric oxide (NO) metabolism might be involved in the induction of lipid peroxidation, as indicated by malondialdehyde (MDA) formation. The purpose of this study was to investigate the behavior of Hcy, NO and MDA in plasma and cerebrospinal fluid (CSF) within 4 days after ischemic stroke onset. Methods: The levels of NO, Hcy and MDA were determined in plasma and CSF on the 3rd or 4th days after the onset of ischemic stroke in 29 patients (12 men and 17 women) and in 13 healthy controls (6 men and 7 women) of comparable age and gender. Results: The plasma MDA, NO and Hcy levels were significantly higher in the stroke patients, while mean MDA, NO and Hcy levels in CSF showed a significant increase in the cases as compared to controls (p<0.01). There were no gender-specific differences in the plasma or CSF MDA, NO and Hcy concentrations. A significant negative correlation was found between duration of diabetes with CSF NO (r=-0.63, p<0.001). The low Glasgow Coma Scale (GKS) was negatively correlated with lethal outcome, (r=-0.76, p<0.001), but it did not correlate significantly with any of the measured parameters. Conclusion: These data support that free radical mechanisms may play a role in the development of brain injury following ischemic stroke. It was suggested that the elevated Hcy may be an important risk factor for acute ischemic cerebral injury.
Highlights
Stroke is the third most common cause of death in industrialized countries, and is a major cause of severe physical disability [1, 2]
The plasma MDA, nitric oxide (NO) and Hcy levels were significantly higher in the stroke patients, while mean MDA, NO and Hcy levels in cerebrospinal fluid (CSF) showed a significant increase in the cases as compared to controls (p
There were no gender-specific differences in the plasma or CSF MDA, NO and Hcy concentrations
Summary
Stroke is the third most common cause of death in industrialized countries, and is a major cause of severe physical disability [1, 2]. Ischemic stroke accounts for 70 to 80% of all strokes. Cerebral infarction may be due to primary thrombosis in an artery or to occlusion of a vessel by an embolus [3]. From the mechanism responsible for the vessel occlusion, ischemia causes a cascade of events that eventually lead to neuronal damage and death [4, 6]. It is generally accepted that oxidative stress means over-generation of reactive oxygen species (ROS) and lipid peroxidation plays an important role in the pathogenesis of neuronal damage induced by ischemia-reperfusion [5].
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