Supplementation with Vitamins C and E Suppresses Leukocyte Oxygen Free Radical Production in Patients with Myocardial Infarction

Supplementation with Vitamins C and E
Suppresses Leukocyte Oxygen Free Radical
Production in Patients
with Myocardial Infarction

This section is compiled by Frank M. Painter, D.C.
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FROM:   European Heart Journal 1995 (Aug);   16(8):   1044–1049

Herbaczynska-Cedro K, K+osiewicz-Wasek B, Cedro K, Wasek W,
Panczenko-Kresowska B, Wartanowicz M

Medical Research Centre,
Polish Academy of Sciences,
Warsaw, Poland

Clinical studies suggest that neutrophil activation during acute myocardial infarction (MI) aggravates tissue injury. Activated neutrophils are an important source of oxygen free radicals (OFR), the injurious effects of which are counteracted by endogenous antioxidants. We have previously shown in healthy subjects that supplementation with antioxidant vitamins C and E suppresses OFR production by isolated neutrophils assayed by chemiluminescence (CL). the present study, performed in patients with acute MI aimed (1) to investigate the effect of vitamin C and E supplementation upon neutrophil OFR production and serum lipid peroxides, (2) to evaluate serum levels of vitamins C and E in the course of MI. Forty–five patients with acute MI were randomized to receive either conventional treatment plus vitamin C and E aa 600–1 p.o. for 14 days (VIT,n=23) or conventional treatment only (control, n=22). All measurements were performed on the 1st and 14th day. Neutrophil OFR production assayed by CL decreased significantly in VIT patients (Wilcoxon test for paired data P<0.01, Chi square test P<0.01). In the control group, changes in OFR production were not significant. Serum lipid peroxides (measured as TBARS) increased in controls (P<0.05), but remained stable in VIT patients. Mean (plus or minusSE) serum ascorbic acid and tocopherol on the 1st day were 0.43 plus or minus 0.18mg% and 3.25 plus or minus 1.32 microM.mM –1 cholesterol, respectively, in all patients. On the 14th day in non–supplemented patients mean tocopherol was unchanged, whereas ascorbic acid increased significantly (0.63 plus or minus 0.24 mg%, P<0.01) suggesting that a low basal level was associated at least in part with the acute phase of the disease. An expected increase in serum vitamin levels occurred in VIT patients. In conclusion, supplementation with vitamins C and E suppresses neutrophil OFR production and lowers the marker of lipid peroxidation in patients with MI. These effects, together with a deficiency of antioxidant vitamins, particularly vitamin C in the early phase of the disease, support the view that supplementation with antioxidant vitamins is advisable in patients with MI.


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