Alterations in plasma lipids, glutathione and homocysteine in relation to dietary copper in rats

Abstract

Magda A. Megahed, Kamel M. A. Hassanin, Ibrahim M. I. Youssef, Abdul Baset A. Elfghi, Kamal A. Amin

Objective: This study aimed to investigate the effect of dietary copper either deficiency or excess on the plasma lipid profile, glutathione (GSH), and homocysteine levels. Design: Three groups of male albino rats were served as control (fed diet containing the required level of Cu; 5.40 mg/kg), copper-deficient (fed diet containing Cu; 0.60 mg/kg) and copper-excess (fed diet containing high level of Cu; 15.0 mg/kg). Materials and Methods: At the end of the experimental period (6 weeks), plasma levels of copper, lipid profile, GSH and homocysteine were estimated in all tested rats groups. Results: There was a significant increase in triacylgycerols, total cholesterol (T.Ch.), high density lipoprotein-cholesterol (HDL-C), very low density lipoproteincholesterol, and low density lipoprotein-cholesterol in rats fed a copperdeficient diet compared to control and those fed copper-excess one. In rats fed copper-deficient, HDL-C/T. Ch. ratio was significantly lower than that of the other tested animals. In addition, plasma GSH increased significantly, while plasma homocysteine decreased significantly in copper-deficient group compared to control and copper-excess groups. A significant negative correlation between plasma copper and each of T.Ch. and plasma GSH was observed in control, copper-deficient and copper-excess groups. On the contrary, plasma copper has shown a significant positive correlation with plasma homocysteine in all groups. Conclusion: the present results indicate that feeding of diets rich in bread and powdered milk develop copper-deficiency that resulted in an increase in plasma T.Ch. and triacylglycerols, while decreased HDL-C/T.Ch. ratio. This is representing a risk factor for the development of cardiovascular disorders. However, the body is able to protect itself against these risky changes by increasing the production of antioxidant (GSH) on the expense of homocysteine. Furthermore, copper supplementation can alleviate these degenerative changes.