Interaction Between Dietary Carbohydrate and Copper Nutriture on Lipid Peroxidation in Rat Tissues

Abstract

The effects of the interactions between dietary carbohydrates and copper deficiency on superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and their roles in peroxidative pathways were investigated. Weanling rats were fed diets deficient in copper and containing either 62% starch, fructose, or glucose. Decreased activity of SOD was noted in all rats fed the copper-deficient diets regardless of the nature of dietary carbohydrate. However, the decreased activity was more pronouced in rats fed fructose. Feeding the fructose diets decreased the activity of GSH-Px by 25 and 50% in the copper-supplemented and copper-deficient rats, respectively, compared to enzyme activities in rats fed similar diets containing either starch or glucose. The decreased SOD and GSH-Px activities in rats fed the fructose diet deficient in copper were associated with increased tissue per-oxidation and decreased hepatic adenosine triphosphate (ATP). When the fructose in the diet of copper-deficient rats was replaced with either starch or glucose, tissue SOD and GSH-Px activities were increased and these increases in enzyme activity were associated with a tendency toward reduced mitochondrial peroxidation when compared to the corre-sponding values for rats fed fructose throughout the experiment Dietary fructose aggrevated the symptoms associated with copper deficiency, but starch or glucose ameliorated them. The protective effects were more pronounced with starch than with glucose.

Essential Trace Elements in Antioxidant Processes

“…Balevska et al (3) reported that when adult rats were fed Cu-deficient diets for 4 wk, there was an increase in hepatic mitochondrial and microsomal lipid peroxidation (as estimated by the formation of lipid hydroperoxides), which was attributed to Cu deficiency-induced reductions in GSH-Px. Subsequent to the work by Balevska et al, other investigators have reported both increased and decreased levels of lipid peroxidation in Cu-deficient animals (4,23,39). For example, Paynter (39) did not find evidence of increased lipid peroxidation (as estimated by thiobarbituric acid reacting substances (TBARS» in rats that were fed diets deficient in Cu but adequate in Se and Mn.…”

Copper deficiency: A potential model for determining the role of mitochondria in cardiac aging

“…Molecular damage caused by reactive oxygen species (ROS) also may contribute to a variety of diseases including cancer, cardiovascular disease, Parkinson's disease, ischemia and chronic inflamation (3,4). Reports showing that copper deficiency in animals increases lipid hydroperoxide content in hepatic mitochondria and microsomes (5), the susceptibility of tissues to lipid peroxidation (6,7), and the production of breath ethane (8) indicate that low copper intake is a dietary condition that causes molecular oxidative damage. In both aging and copper deficiency, the suppression of antioxidant enzyme activities may increase oxidative stress and facilitate damage by ROS (9,10).…”

Low dietary iron restores functional capabilities of both exocrine and endocrine pancreas in copper-deficient rats

“…Copper deficiency is associated with reduced activity of antioxidant enzymes [12]. Changes in pancreatic antioxidant enzymes are thought to be involved in the development of insulin-dependent diabetes mellitus [34][35][36].…”

“…Blood was collected for hematocrit measurement and measurements of plasma insulin. Other liver portions were removed for the assessment of lipid peroxidation by measuring malondialdehyde formation using the thiobarbituric acid (TBA) reaction technique as previously described [12].…”