Vitamin C Research Today is a free monthly online journal that collates and summarizes the latest research about Vitamin C, including details on benefits, dosage, supplements, information. | ||||||||
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Smoking-induced monocyte dysfunction is reversed by vitamin C supplementation in vivo.Stadler N, Eggermann J, Vöö S, Kranz A, Waltenberger J Department of Cardiology, University of Maastricht, Cardiovascular Research Institute of Maastricht, P. Debyelaan 25, NL-6202 AZ Maastricht, The Netherlands. OBJECTIVE: The role of antioxidants in preventing vascular disease remains controversial. Vascular endothelial growth factor (VEGF-A) is important for endothelial and monocyte function. This study investigated the negative effects of smoking on monocyte migratory responsiveness to VEGF-A and the usefulness of vitamin C to prevent smoking-induced monocyte dysfunction. METHODS AND RESULTS: The chemotactic response of isolated monocytes from a cohort of 17 non-smokers and 10 smokers toward VEGF-A was assessed. VEGF-A significantly stimulated the migration of monocytes in non-smokers; the monocytes from smokers failed to respond to VEGF-A. Repeated analysis after 2 weeks of vitamin C intake (2 g/d) showed a fully restored VEGF-A-induced monocyte migration in smokers. VEGF-A serum levels were not altered by vitamin C. VEGF-A-inducible kinase activity was intact in monocytes from smokers as assessed by in vitro kinase assay. Monocyte dysfunction can be mimicked in vitro by challenging monocytes with a range of reactive oxygen species (ROS). CONCLUSIONS: Stimulation of monocyte migration by VEGF-A was severely attenuated in smokers, and the deficit observed was surmounted by vitamin C supplementation. The negative effects of smoking on monocyte function may translate into adverse impacts on VEGF-A-dependent repair processes such as arteriogenesis. These results propose a causative role of oxidative stress in smoking-induced monocyte dysfunction. Published 22 December 2006 in Arterioscler Thromb Vasc Biol, 27(1): 120-6.
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