Superoxide Dismutase Activity in Copper-Deficient Swine

Williams, Dennis; Lynch, Robert E.; Lee, G. R.; Cartwright, G. E.

doi:10.3181/00379727-149-38844

Cited by 67 publications

(13 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Secondly, the copper-zinccontaining enzyme superoxide dismutase has shown an extremely significant anti-inflammatory activity in vivo, both in man [28] and animals [21,28,29]. Thirdly, BOHNENKAMP and WESER [33], using a 0.2 p.p.m, copper-deficient diet, were able to show a remarkable decrease of copper-zinc superoxide dismutase activity of the total blood cells in copper-deprived rats (about 50% decrease after 1 month of diet); similar results were also obtained in copper-deficient pigs [34].…”

Section: Discussion"supporting

confidence: 60%

Concerning the role of endogenous copper in the acute inflammatory process

Milanino¹,

Conforti²,

Fracasso³

et al. 1979

Agents and Actions

View full text Add to dashboard Cite

The development of two models of acute inflammation (carrageenan-induced foot oedema and pleurisy) was studied in rats after 1 month of a 0.2 p.p.m. copper-deficient diet and after 5 months of a 0.6-0.8 p.p.m. copper-deficient diet. A 'pro-inflammatory' effect of copper deficiency was observed with the 0.2 p.p.m. diet, whilst no effect was evident following the 0.6-0.8 p.p.m. copper deficient diet. These results are briefly commented upon.

show abstract

Section: Discussion"supporting

confidence: 60%

Concerning the role of endogenous copper in the acute inflammatory process

Milanino¹,

Conforti²,

Fracasso³

et al. 1979

Agents and Actions

View full text Add to dashboard Cite

show abstract

“…Cu,Zn-SOD contains 60% of copper in the erythrocytes [11]. A low level of erythrocyte Cu,Zn-SOD may accelerate the membrane defect because of a decreased capacity to dispose of superoxide [12]. Our pa tient had a low Cu,Zn-SOD acitivity in the erythrocytes as compared with healthy subjects, and the life span of her erythrocytes was shortened.…”

Section: Discussionmentioning

confidence: 96%

Anemia and Neutropenia in a Case of Copper Deficiency: Role of Copper in Normal Hematopoiesis

et al. 1992

View full text Add to dashboard Cite

We present a patient who developed severe anemia and neutropenia after receiving parenteral nutrition for 2.5 years. The serum levels of copper and ceruloplasmin were low, and the bone marrow showed the presence of ringed sideroblasts and vacuolated immature cells. The administration of copper chloride by bolus injection led to a rapid improvement in anemia and neutropenia. The number of progenitor cells (colony-forming unit-granulocyte-macrophage and erythrocyte) present before the copper supplementation was well preserved. It is therefore suggested that copper enzymes play an important role in the maturation of hematopoietic cells.

show abstract

“…This decrease correlated strongly with the down-regulation of both SOD1 expression (30%) and activity (70%). A reduction in erythrocyte SOD1 activity in response to dietary copper deficiency has been described in various mammalian species [53]–[55] including mice [39]. Obviously, altered functioning of Cu,Zn-SOD increases the risk of oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Haemolysis and Perturbations in the Systemic Iron Metabolism of Suckling, Copper-Deficient Mosaic Mutant Mice – An Animal Model of Menkes Disease

et al. 2014

View full text Add to dashboard Cite

The biological interaction between copper and iron is best exemplified by the decreased activity of multicopper ferroxidases under conditions of copper deficiency that limits the availability of iron for erythropoiesis. However, little is known about how copper deficiency affects iron homeostasis through alteration of the activity of other copper-containing proteins, not directly connected with iron metabolism, such as superoxide dismutase 1 (SOD1). This antioxidant enzyme scavenges the superoxide anion, a reactive oxygen species contributing to the toxicity of iron via the Fenton reaction. Here, we analyzed changes in the systemic iron metabolism using an animal model of Menkes disease: copper-deficient mosaic mutant mice with dysfunction of the ATP7A copper transporter. We found that the erythrocytes of these mutants are copper-deficient, display decreased SOD1 activity/expression and have cell membrane abnormalities. In consequence, the mosaic mice show evidence of haemolysis accompanied by haptoglobin-dependent elimination of haemoglobin (Hb) from the circulation, as well as the induction of haem oxygenase 1 (HO1) in the liver and kidney. Moreover, the hepcidin-ferroportin regulatory axis is strongly affected in mosaic mice. These findings indicate that haemolysis is an additional pathogenic factor in a mouse model of Menkes diseases and provides evidence of a new indirect connection between copper deficiency and iron metabolism.

show abstract

Superoxide Dismutase Activity in Copper-Deficient Swine

Cited by 67 publications

References 0 publications

Concerning the role of endogenous copper in the acute inflammatory process

Concerning the role of endogenous copper in the acute inflammatory process

Anemia and Neutropenia in a Case of Copper Deficiency: Role of Copper in Normal Hematopoiesis

Haemolysis and Perturbations in the Systemic Iron Metabolism of Suckling, Copper-Deficient Mosaic Mutant Mice – An Animal Model of Menkes Disease

Contact Info

Product

Resources

About