Despite convincing in vitro evidence, a vitamin C±E interaction has not been con®rmed in vivo. This study was designed to examine the effects of supplementation with either vitamin C or E on their respective plasma concentrations, other antioxidants, lipids and some haemostatic variables. Fasting blood was collected before and after intervention from thirty healthy adults in a doubleblinded crossover study. Baselines for measured variables were established after 2 weeks of placebo supplementation, followed by daily supplementation with 73×5 mg RRR-a-tocopherol acetate or 500 mg ascorbic acid, and placebo, for 6 weeks. A 2 month washout preceded supplement crossover. Mean values showed that plasma lipid standardised a-tocopherol increased with ascorbic acid supplementation: from 4×09 (SEM 0×51) to 4×53 (SEM 0×66) mmol/ mmol total cholesterol plus triacylglycerol (P , 0×05), and plasma ascorbic acid increased from 62×8 (SEM 14×9) to 101×3 (SEM 22×2) mmol/l (P , 0×005). Supplementation with (RRR)-atocopherol acetate increased plasma a-tocopherol from 26×8 (SEM 3×9) to 32×2 (SEM 3×8) mmol/l (P , 0×05), and lipid-standardised a-tocopherol from 4×12 (SEM 0×48) to 5×38 (SEM 0×52) mmol/ mmol (P , 0×001). Mean plasma ascorbic acid also increased with vitamin E supplementation, from 64×4 (SEM 13×3) to 76×4 (SEM 18×4) mmol/l (P , 0×05). Plasma ferric reducing (antioxidant) power and glutathione peroxidase (U/g haemoglobin) increased in both groups, while urate, total cholesterol and triacylglycerol levels decreased (P , 0×05 throughout). Results are supportive of an in vivo interaction between vitamins C and E.

Copper is an essential trace element in the maintenance of the cardiovascular system. Copper-deficient diets can elicit, in animals, structural and functional changes that are comparable to those observed in coronary heart disease. In this study, the effect of dietary-induced copper deficiency on aortic lesion development was measured by quantitative image analysis in C57BL/6 mice that are susceptible to diet-induced aortic lesions. The diets administered were severely copper deficient (0.2 mg/kg diet), marginally deficient (0.6 mg/kg diet), or copper adequate (6.0 mg/kg diet). Similarly, increased aortic lesion areas and elevated serum cholesterol were demonstrated in both deficient groups, compared with the copper-adequate group. Evidence for graded differences in copper status among the dietary groups was shown by the dose-response increase in liver copper concentration, copper-zinc superoxide dismutase and cytochrome-c oxidase activities, together with serum caeruloplasmin oxidase with increasing intakes of dietary copper. Despite the difference in copper status between the copper marginal and severely deficient groups, similar lesions found in both groups of mice suggest a threshold effect of copper deficiency on lesion formation.

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