Antioxidant Status, Proinflammatory Cytokines, and Acute-Phase Protein Response in Smokers after Myocardial Infarction.
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Lipid peroxidation and inflammatory response were studied in smokers and non-smokers after myocardial infarction (MI). The MI group studied included 18 smokers and 15 non-smokers, and 20 smokers without vascular complications served as controls. The results obtained showed that in both smokers and non-smokers the onset of MI brought about a reduction (p<0.001) in the erythrocyte antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase, and catalase) and antioxidant scavenger levels (vitamins A, C, and E and reduced glutathione). Lipid peroxide level measured in terms of thiobarbituric acid-reactive substances increased by several fold (p<0.001). Levels of proinflammatory cytokines (interleukin-1β, interleukin-6, and tumor necrosis factor-α) and acute-phase proteins (plasma-acid glycoprotein, 2-macroglobulin, C-reactive protein, and ceruloplasmin) were also increased by several fold (p<0.001). Though alterations were observed in smokers as well as non-smokers after an episode of MI the percentage of alterations observed was higher in the smokers. This may be due to the smoking-induced free radical production in the presence of decreased antioxidant status, which, in turn, enhances lipid peroxidation and inflammatory responses. Hence, the data suggest that smokers may benefit from oral supplementation with antioxidant vitamins to alleviate smoking-induced free radical damage and inflammatory responses.
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