The effect of dietary copper (Cu) deficiency on the antioxidant enzyme superoxide dismutase (SOD) was investigated in both erythrocyte and liver samples of 40 weanling Wistar rats. Groups were fed control (10 mg Cu/kg) or Cu-deficient (0.5 mg Cu/kg) diets for 7 wk. In this study, dietary copper deficiency did not affect growth, food intake, liver size, or hemoglobin levels. Protein concentrations were considerably decreased in the livers of the copper-deficient group compared to control groups after 7 wk. Erythrocyte SOD activity was not significantly different in copper-deficient groups. In contrast, SOD activity was significantly reduced in livers of rats consuming the Cu-deficient diet compared to controls. The in vitro SOD activities in the presence of five different macro-cyclic copper-II containing complexes with different stability constants were studied. The moderately stable copper complex increased the SOD activity in Cu-deficient liver and erythrocyte samples only at wk 7. At wk 6, a significant increase in SOD activity in liver samples only was observed. In contrast, at wk 4, no significant differences in SOD activity were observed upon addition of Cu complexes. These results suggest that the increase in SOD activity may be due to superoxide-like action or other properties of this copper complex.