Decreased levels of plasma vitamin C and increased concentrations of inflammatory and oxidative stress markers after stroke.
OBJECTIVE
Inflammatory response is a critical component of the complex pathophysiological response to stroke. Vitamin C has been shown to have important roles in cell performance and vascular function. In this study, we compared the nutritional status and levels of inflammatory markers between stroke cases and controls and assessed which antioxidant was associated with levels of inflammatory markers and oxidative stress among cases and controls.


METHODS
We evaluated the nutritional status and measured plasma levels of vitamins C and E, uric acid, serum levels of C-reactive protein (CRP), the cytokines tumor necrosis factor-alpha and interleukin-1beta, intercellular adhesion molecule-1 (ICAM-1) and chemokine monocyte chemoattractant protein-1 (MCP-1), prostaglandins PGE2 and PGI2, and 8-isoprostanes (8-epiPGF2alpha) for 15 patients with ischemic stroke within 2 to 5 days after stroke onset and for 24 control subjects.


RESULTS
Stroke patients had significantly lower plasma levels of vitamin C than did controls. Among stroke patients, CRP was significantly elevated, as were the ICAM-1, MCP-1, and 8-epiPGF2alpha, but the prostaglandins PGE2 and PGI2 were significantly reduced. Interestingly, vitamin C concentration was significantly inversely correlated with the levels of CRP and 8-epiPGF2alpha among stroke patients, and 8-epiPGF2alpha was significantly associated with the levels of CRP. Uric acid was also elevated among stroke patients.


CONCLUSIONS
Lower vitamin C concentration, higher serum levels of inflammatory (CRP, ICAM-1, MCP-1) and oxidative stress (8-epiPGF2alpha) markers, and lower PGI2 and PGE2 concentrations among stroke patients indicate the presence of an inflammatory response associated with stroke.
Sánchez-Moreno
Concepción
C
Nutrition and Neurocognition Laboratory, Jean Mayer USDA-Human Nutrition Research Center on Aging, Boston, Mass 02111, USA.
Dashe
John F
JF
Scott
Tammy
T
Thaler
David
D
Folstein
Marshal F
MF
Martin
Antonio
A
D000368:Aged; D000975:Antioxidants / Q000032:analysis; D001205:Ascorbic Acid / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D002545:Brain Ischemia / Q000097:blood* / Q000150:complications; D002097:C-Reactive Protein / Q000032:analysis; D018932:Chemokine CCL2 / Q000097:blood; D016207:Cytokines / Q000097:blood; D004032:Diet; D015237:Dinoprost / Q000031:analogs & derivatives* / Q000097:blood; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008875:Middle Aged; D009483:Neuropsychological Tests; D009752:Nutritional Status; D018384:Oxidative Stress; D011453:Prostaglandins / Q000097:blood; D012016:Reference Values; D020521:Stroke / Q000097:blood* / Q000150:complications; D013997:Time Factors; D014527:Uric Acid / Q000097:blood; D014810:Vitamin E / Q000097:blood
D000975:Antioxidants; D015415:Biomarkers; D018932:Chemokine CCL2; D016207:Cytokines; D018836:Inflammation Mediators; D011453:Prostaglandins; D018799:Intercellular Adhesion Molecule-1; D014810:Vitamin E; D014527:Uric Acid; C075750:8-epi-prostaglandin F2alpha; D002097:C-Reactive Protein; D015237:Dinoprost; D001205:Ascorbic Acid