Development Of Copper Deficiency Research Articles

The influence of gender on developing copper deficiency and on free radical generation of rats fed a fructose diet

The present investigation was conducted to determine whether differences in copper and iron status between male and female rats can be detected during the development of copper deficiency. These differences may explain the protection of the female against the severity of copper deficiency. In addition, the livers of all rats were exposed to electron-spin resonance (ESR) spectroscopy for the presence of free radicals. Male and female rats were fed from weaning either copper-deficient or -adequate diets containing fructose for 31 days. Rats were killed at day 0, 8, 16, 24, and 31 of the study. Throughout the study, copper-deficient males exhibited the same organ copper concentrations as copper-deficient female rats. However, only in the male did copper deficiency cause a reduction in body weight and an increase in liver and heart sizes but a decrease in pancreas size. In contrast, organ iron concentrations were different between males and females. Only copper-deficient males were anemic. Only the livers of copper-deficient males showed the presence of free radicals. Although the livers of copper-deficient female rats exhibited higher concentrations of hepatic iron than their male counterparts, their livers did not show the presence of free radicals. The data of the present study suggest that changes in organ sizes and the severity of copper deficiency are not solely due to the total concentrations of iron and/or copper. The type of iron compound and the presence of free radicals may be involved in the pathology of copper deficiency of the male.

Effects of Dietary Tin and Copper on Rat Hepatocellular Antioxidant Protection

The effects of dietary tin on copper status and on enzymes and metabolites involved in hepatocellular antioxidant protection were measured in rats fed copper-adequate or copper-deficient diets with glucose or fructose. Rats became copper-depleted after 4 weeks on diets containing less than 0.5 micrograms of copper/g as evidenced by significant decreases in liver copper and serum ceruloplasmin. Signs of copper deficiency occurred in copper-depleted rats fed diets containing 100 micrograms of tin/g. Significant effects of tin on liver glutathione peroxidase and superoxide dismutase activities and on liver iron and total glutathione concentrations were observed. Interactions between copper and tin on liver copper and iron and on liver superoxide dismutase and malondialdehyde production are reported. Adverse effects of feeding diets containing 100 micrograms of tin/g include (i) copper depletion in rats fed copper-adequate diets, (ii) accelerated development of copper deficiency in rats fed copper-deficient diets, and (iii) reduction in hepatocellular antioxidant protection.

Development of copper deficiency in neonatal mice

Dietary copper (Cu) deficiency was produced in Swiss albino mice to determine the temporal relationship between depletion of Cu and changes in the cardiovascular and nervous system. Dams were placed on a Cu-deficient diet 4 days after parturition. Half the dams were provided with deionized water and their offspring are referred to as Cu-deficient (−Cu). Half the dams were given cupric sulfate in their drinking water (20 μg Cu/mL) and their offspring are referred to as Cu-adequate (+Cu). At 6 weeks of age a sample of the −Cu mice were repleted with CuSO 4. Mice were sampled 1 day after birth and at weekly intervals for 7 weeks. Both +Cu and −Cu mice grew at the same rate: birth weight increased 16-fold at 6 weeks of age. Liver Cu more than doubled between 1 and 7 days of age. At 2 weeks of age −Cu mice were anemic (lower hematocrit and hemoglobin) and had lower liver Cu and plasma ceruloplasmin activity compared to +Cu mice. Liver Fe was not elevated in −Cu mice until 2 weeks after anemia developed. At weaning first signs of altered catecholamine metabolism included elevation of dopamine in both heart and spleen. Norepinephrine concentrations and content, in contrast, were not both lowered in −Cu mice until 5 weeks of age. Heart weight was first elevated in −Cu mice at 6 weeks of age and relative weight (mg/g body wt) at 4 weeks of age. Liver Cu concentration was lower in 1-week repleted mice than in +Cu mice. Anemia preceded the development of cardiac hypertrophy and altered catecholamine levels in −Cu mice.

Interaction of Dietary Carbohydrate, Ascorbic Acid and Copper with the Development of Copper Deficiency in Rats

The effects of dietary carbohydrate and ascorbic acid on the development of copper deficiency were investigated. Male Sprague-Dawley rats (n = 48) were fed one of eight diets in a 2 × 2 × 2 factorial design for 21 d. These diets varied in copper (1.11 or 8.96 µg Cu/g diet), carbohydrate (sucrose or cornstarch, 62.3%) and ascorbic acid (0 or 1%). Compared to controls, copper-deficient rats had lower hematocrit and ceruloplasmin levels, lower levels of copper and iron in several tissues, higher heart weights and lower spleen weights. During copper deficiency, liver iron levels were higher than control levels when cornstarch, but not sucrose, was the carbohydrate source, while liver and gastrointestinal tract weights were higher with sucrose compared to cornstarch. Copper-deficient rats fed ascorbic acid had significantly (P < 0.05) lower hematocrits when fed sucrose compared to starch [29.6 ± 1.2 vs. 36.8 ± 1.2 g/dl (mean ± SEM), respectively]. In copper-deficient rats, sucrose tended to lower the apparent absorption of copper compared to cornstarch, while ascorbic acid reduced the apparent absorption of iron. Thus, sucrose and ascorbic acid appeared to reduce hematocrit levels through effects on mineral absorption.

Development of copper deficiency in rats fed fructose or starch: weekly measurements of copper indices in blood.

Copper deficiency was induced in weanling rats fed diets whose sole source of carbohydrates was starch or fructose for 7 weeks. Conventional parameters of copper status, plasma copper concentrations, ceruloplasmin activity, and erythrocyte superoxide dismutase (SOD) activity were longitudinally monitored weekly to follow the development of the deficiency and to correlate these indices with the degree of severity of the deficiency. Although 30% of the rats fed a copper-deficient fructose diet died and no deaths occurred in rats fed the copper-deficient starch diet, plasma copper, ceruloplasmin, and SOD activities were reduced to a similar extent in all rats fed copper-deficient diets regardless of the type of dietary carbohydrate. Thus, none of the indices used accurately reflected the greater degree of deficiency or mortality in rats fed the fructose diet deficient in copper. The results of the present study underscore the need for more sensitive tests or alternative parameters to assess copper status in living animals.

Copper Deficiency in Infants with Active Celiac Disease

SummaryCeliac disease was diagnosed in two unrelated infants aged 7 and 7.5 months with severe malnutrition. They showed typical clinical, biological, and histological signs of the disease. Moreover, accompanying copper deficiency was suggested by severe hypocupremia and persistent neutropenia; bone radiographs were also compatible with this diagnosis. Rapid and complete correction of these anomalies could only be obtained after addition of oral copper sulfate to the gluten free diet. Mechanisms possibly involved in the development of copper deficiency in young infants with celiac disease are: (a) chronic malabsorption; (b) high copper needs in rapidly growing infants; and (c) possibly increased biliary and digestive losses. It is therefore suggested that young children with severe celiac disease should be monitored for their copper status.

Metabolic interactions of copper with other trace elements.

Metabolic interactions between copper and other trace elements influence not only the susceptibility of animals and humans to deficiency or toxicity of copper but also the biochemical and pathological consequences of these states. Antagonistic trace elements affect the utilization of copper by reducing its solubility within the intestinal lumen, by competing with copper during its absorption or transport, or by modifying its distribution between receptors in body tissues. The derangement of iron-dependent functions during the development of copper deficiency provides a further example of such interactions which, in this instance, arise from the involvement of copper in processes that apparently regulate the flux of iron between plasma and cellular pools. This paper deals with recent studies of the mechanisms of the interactions between copper and zinc, cadmium molybdenum and iron.

An evaluation of five varieties ofLotus pedunculatusCav. compared with ‘Grasslands Huia’ white clover under grazing at Kaikohe

Abstract A 5-year evaluation of five lotus varieties under moderately hard sheep grazing was conducted at Kaikohe on Wharekohe silt loam. Best overall performance was from two diploid varieties containing Portuguese material (G4703 and G4704). Summer growth of all lotus varieties was better than ‘Grasslands Huia’ white clover and those with a higher New Zealand content were best (G4701, G4702, and G4703). Winter growth from varieties with Portuguese content (G4703, G4704, and G4705) was better than that of the other varieties and Huia. The diploid varieties G4703 and G4704 performed as well as Huia in spring and autumn. Ryegrass growth was best with Huia, over the first 2 years, until the development of copper deficiency which resulted in a large loss of legume vigour and total growth, particularly in Huia-based pastures. In the fourth year this deficiency was corrected and legume growth, particularly Huia, recovered. A change in grazing management in the last year suggested that the more erect varieties (G4702, G4704, and G4705) may perform better under rotational grazing.

Production of copper deficiency in the rat by an egg albumin diet.

SummaryCopper deficiency as judged by achromotrichia and lower levels of copper in blood, plasma, liver, kidney, brain, and hair was induced in black rats by feeding a copper-deficient diet containing egg albumin. Results obtained with this diet were comparable to those obtained with a skim milk copper-deficient diet. Ascorbic acid, at 1% of the diet, had no effect on the development of copper deficiency in rats fed the egg albumin diet. Soybean protein diets were ineffective in producing copper deficiency. Plasma protein patterns obtained by disc electrophoresis were not influenced by copper deficiency.