Oxidative stress in the chronic phase after stroke.
The spontaneous and the stimulated extracellular generation of reactive oxygen species (ROS) by peripheral phagocytes, the blood antioxidant capacity and the degree of oxidative damage were evaluated in patients with severe ischemic and hemorrhagic stroke in the chronic phase of disease. It was found in patients compared to the control group that: (i) the spontaneous phagocyte oxidative activity was enhanced independently of the type of stroke and the time elapsed after stroke onset; (ii) there was no difference in the extracellular ROS generation stimulated by opsonin-dependent and independent receptor mechanisms; (iii) there was no change in the indices of blood antioxidant capacity; (iv) the concentration of plasma lipid peroxides was enhanced regardless of the type of stroke, but it significantly increased over time; and (v) the concentration of blood thiobarbituric acid-reactive material was also enhanced. It was independent of the type of stroke and remained elevated during the whole period studied. We have demonstrated an enhanced spontaneous phagocyte oxidative activity and oxidative damage to lipids in patients in the chronic phase after stroke. The elimination of generated ROS and products of lipid peroxidation from the circulation could prevent the aggravation of chronic vascular injury in patients and could reduce the possibility of a subsequent stroke. This suggests the need for complex therapy, including antioxidant treatment directed to exclude the effects of free radicals, after the oxidative stress of stroke.
Alexandrova
Margarita L
ML
Department of Biophysics, Medical University, Pleven, Bulgaria. margalexandrova@hotmail.com
Bochev
Petyo G
PG
Markova
Vanya I
VI
Bechev
Blagovest G
BG
Popova
Marina A
MA
Danovska
Maya P
MP
Simeonova
Virginia K
VK
D000975:Antioxidants / Q000378:metabolism*; D016022:Case-Control Studies; D002908:Chronic Disease; D005260:Female; D006801:Humans; D015227:Lipid Peroxidation; D008297:Male; D008875:Middle Aged; D009895:Opsonin Proteins / Q000378:metabolism; D018384:Oxidative Stress; D010586:Phagocytes / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D011971:Receptors, Immunologic / Q000378:metabolism; D012307:Risk Factors; D020521:Stroke / Q000378:metabolism* / Q000503:physiopathology; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D000975:Antioxidants; D009895:Opsonin Proteins; D017382:Reactive Oxygen Species; D011971:Receptors, Immunologic; D017392:Thiobarbituric Acid Reactive Substances; C091196:opsonin receptor