Copper toxicosis

In mammals, copper absorption across the intestinal mucosa is inhibited by concomitant high oral intake of zinc (Aaseth and Norseth 1986). In livers from Weddell seals, copper is positively correlated with zinc (Szefer et al. 1994). The addition of zinc to swine diets protects against copper toxicosis caused by eating diets containing 250 mg Cu/kg ration (USEPA 1980). 

In domestic pigs, copper toxicosis results from eating diets containing 250 mg Cu/kg ration and is characterized by anemia, jaundice, elevated levels of Cu in serum and liver, and elevated serum AAT activity (USEPA 1980). Shortly before death, copper-poisoned pigs had white noses, poor balance, stomach histopathology, orange cirrhotic livers, anorexia, and anemia (Higgins 1981). 

The relation between copper toxicosis, copper absorption rates, and copper retention (Stokes 1979 ATSDR 1990)... 

In acute copper toxicosis (378), peritoneal dialysis has also been successfully implemented with simultaneous administration of penicillamine. In order to bridge the time until hver transplantation can be carried out, plasmapheresis and haemofiltrations are recommended. 

Sternlieb, I. Hepatic copper toxicosis. J. Gastroenterol. Hepatol. 1989 4 175-181... 

Price LA, Walker NI, Clague AE, Pullen ID, Smits SJ, Ong TH, Patrick M. Chronic copper toxicosis presenting as liver failure in an Australian child. Pathology 1996 28(4) 316-20. 

Sokol RJ, Twedt D> McKim JM Jr, Devereaux MW, Karrer FM, Kami I, et al. Oxidant injury to hepatic mitochondria iri patients with Wilson s disease aiid Bedlington terriers with copper toxicosis. Gastroenterology 1994 107 1788-98. 

MuEer T, Muller W, Feichtinger H. Idiopathic copper toxicosis. Am J Clin Nutr 1998 67 1082S-6S. 

Proschowsky et al. (2000) have developed a diagnostic test based on the micro satellite marker C04107 for copper toxicosis in Bedlington terriers described by Yuzbasiyan et al. (1997). Until now, this test has to be considered the best tool that breeders of Bedlington terriers can use in the eradication of copper toxicosis, as surveys carried out so far have indicated that the genetic basis for the disease is similar both in Europe and in the USA. 

Biempica L, Raugh H, Quintana N and Stern-LiEB I (1988) Morphological and chemical studies on a murine mutation (toxic milk) resultingin hepatic copper toxicosis. Lab Invest 59 500- 508. 

Brewer GJ, Dick RD, Schall W, Yuzbasiyan -Gurkan V, MulianeyTP, Pace C, Lindgren J, Thomas M and Padgett G (1992) Use of zinc acetate to treat copper toxicosis in dogs. J Am Vet Med Assoc 201 564-568. 

Hunt DM, Wake SA, Merger JF and Danks DM (1986) A study of the role of metaUothionein in the inherited copper toxicosis of dogs. Biochem J 236 409 -415. 

Johnson GF, Stfenlifb I, Twfdt DC, Geushoff PS and ScHFiNBFEG IH (1980) Inheritance of copper toxicosis in Bedlington terriers. Am J Vet Res 41 1865-1866. 

Propping P (1980) Neue Entwicklungen in der Pharmakogenetik. Klinikarzt 9 422-434. Prosghowsky he, Jepsen B, Jensen HE, Jensen AL and Fredholm M (2000) Microsatellite marker C04107 as a diagnostic marker for copper toxicosis in the danish population of Bedlington terriers. Acta Vet Scand 41 345-350. 

Twedt DC, Sternlieb 1 and Gilderson SR (1979) Clinical, morphologic and chemical studies on copper toxicosis of Bedlington terriers. J Am Vet Med Assoc 175 269-275. 

Yuzbasiyan-Gurkan V, Blanton SH, Cao Y, Ferguson P, Li j, Venta PJ and Brewer GJ (1997) Linkage of a microsatellite marker to the canine copper toxicosis locus in Bedlington terriers. Am J Vet Res 58 1-5. 

Yuzbasiyan-Gurkan V, Wagnitz S, Blanton SH and Brewer GJ (1993) Linkage studies of the esterase D and retinoblastoma genes to copper toxicosis a moddfor Wilson disease. Genomics 15 86-90. 

In animals, copper plays some specific physiological roles, forming part of many proteins, e.g. the enzymes ceruloplasmin, monoamine oxidase, superoxide dismutase (SOD) and cytochrome c oxidase. Copper deficiency is a more common metabolic alteration than copper toxicosis and anemia is the common expression in most of the studied species. Ruminants appear to be particularly susceptible to copper toxicity and are the only animals in which significant, even lethal, effects can occur (Davis and Mertz, 1986). According to Davis and Mertz (1986), the normal range of copper in the blood of healthy animals is 0.5-1.5 (Jig/ml. However, Minoia et al. (1990) report a slightly different range in humans, from 0.535 to 1.94 jLg/ml. In mammalian blood, 50% of the copper is usually contained in the erythrocytes, where it appears to be more or less firmly bound (Davis and Mertz, 1986). 

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