Background: Copper deficiency induces a dramatic decrease of superoxide dismutase activity and leads to alteration of antioxidant defense systems.
Methods: and
Objective: Experiments were conducted in weanling male, intact and ovariectomized female rats, fed either a copper-adequate or copper-deficient diet for seven weeks, in order to determine whether endogenous estrogen could modulate oxidative stress and the severity of copper-deficiency.
Results: Feeding male rats a copper-deficient diet induced typical signs of copper deficiency, such as decreased hepatic copper, growth retardation, anemia, heart hypertrophy, pancreas atrophy and hypercholesterolemia. Furthermore, copper deficiency increased the amount of lipid peroxidation products in the heart, liver and pancreas following in vitro iron induction. Although levels of hepatic copper in copper-deficient females were similar to those of their male counterparts, the females were partially protected from the adverse effects of the deficiency (no growth retardation, less severe anemia, lesser extent of lipid peroxidation). Thus, female rats are provided with a greater degree of protection against oxidative damage than males. However, females did not appear to be protected against pancreas atrophy, heart enlargement and hypercholesterolemia induced by copper deficiency. This observed partial protection of females was lost after ovariectomy as shown by decreased body weight and hematocrit, heart enlargement and higher tissue peroxidation in ovariectomized females compared to intact females.
Conclusions: The results suggest that the partial protection of copper deficient females is related to the antioxidant properties of estrogens. The protective action of estrogen against oxidative stress is of particular importance when antioxidant defenses are decreased as shown in this experimental model.