Kidney copper

In mammals, phenobarbital and phenytoin increase serum ceruloplasmin concentrations (Aaseth and Norseth 1986). Chronic copper poisoning in sheep is exacerbated when diets contain heliotrope plants (Heliotropium sp., Echium spp., Senecio sp.). Aggravated effects of the heliotrope plants include reduced survival and a twofold to threefold increase in liver and kidney copper concentrations when compared to control animals fed copper without heliotropes (Howell et al. 1991). Rats given acutely toxic doses of 2,3,7,8-tetrachlorodibenzo-para-dioxin had elevated concentrations of copper in liver and kidney because of impaired biliary excretion of copper (Elsenhans et al. 1991). Morphine increases copper concentrations in the central nervous system of rats, and dithiocarbam-ates inhibit biliary excretion (Aaseth and Norseth 1986). In human patients, urinary excretion of copper is increased after treatment with D-penicillamine, calcium disodium EDTA, or calcium trisodium diethylenetriamine penta acetic acid (Flora 1991). 

In Poland near copper foundries, livers from cattle (Bos sp.) have higher copper concentrations (35 to 140 mg/kg FW) than cattle from agricultural regions (7 to 32 mg/kg FW) however, kidney copper concentrations are comparable for both regions (Falandysz 1993a). Cattle found dead in South Africa near a copper smelter have elevated levels of copper in liver (600 mg/kg FW ... 

No deaths. After 32 days whole fish contained 1.5 mg/kg FW vs. 1.2 at start copper concentrations were elevated in gill, gut, blood, skin, and mucus, but not in muscle, liver, or kidney. Copper concentrations in gill and kidney tissues were elevated 12 days after exposure, but other tissues were normal... 

All adole.scents or young adults wdth otherwise unexplained neurological or hepatic disease should be investigated for Wilson s disease, since this condition is fatal if not diagnosed and treated. Symptoms are a result of copper deptisi-lion in liver, brain, and kidney. Copper deposits in the eye can. sometimes be seen as a brown pigment around the iris (the Kayser-Fleischer ring). 

The large kidney copper content, 270 pg/g of tissue ash, when compared with the very small urine copper content, 0.04 pg/ml, suggests a conservatory role for the kidney. Gastric, intestinal and adrenal tissues also have high copper content, 200 to 300 /ig/g of tissue ash, and this reflects their high metabolic rates. Remaining tissues have lesser amounts of copper because of their relatively lower metabolic activity, but it is just as important for normal metabolism in these tissues as it is in all others. 

Diagnosis is based on history, clinical signs and lesions, and confirmation of elevated copper levels in the gastrointestinal contents or kidney. Copper levels in the liver and blood ate not usually increased. 

Liver and kidney copper lev greater than 150 ppm and 15 ppm, respectively, (wet-weight basis) are associated with copper toxicosis. 

Copper. AH human tissues contain copper. The highest amounts are found in the Hver, brain, heart, and kidney (102). In blood, plasma and erythrocytes contain almost equal amounts of copper, ie, ca 110 and 115 mg/100 mL, respectively. 

Lead Incineration, smelting and casting, transportation. Copper and lead smelting, MSWs Neurological impairments kidney, hver, and heart damage. 

Copper 1.3 TT Action Level = 1.3 Short term exposure Gastrointestinal distress. Long term exposure Liver or kidney damage. Corrosion of hou.sehold plumbing systems erosion of natural deposits... 

Wimd-klee, m. kidney vetch, -kraut, n. vulnerary pknt. -pulver, n. vulnerary powder, -salt, m. wound exudate, -schwamm, m. surgeon s agaric, -stein, m. copper alumi-nate. 

Copper is an essential trace element. It is required in the diet because it is the metal cofactor for a variety of enzymes (see Table 50—5). Copper accepts and donates electrons and is involved in reactions involving dismu-tation, hydroxylation, and oxygenation. However, excess copper can cause problems because it can oxidize proteins and hpids, bind to nucleic acids, and enhance the production of free radicals. It is thus important to have mechanisms that will maintain the amount of copper in the body within normal hmits. The body of the normal adult contains about 100 mg of copper, located mostly in bone, liver, kidney, and muscle. The daily intake of copper is about 2—A mg, with about 50% being absorbed in the stomach and upper small intestine and the remainder excreted in the feces. Copper is carried to the liver bound to albumin, taken up by liver cells, and part of it is excreted in the bile. Copper also leaves the liver attached to ceruloplasmin, which is synthesized in that organ. 

Metallothioneins are a group of small proteins (about 6.5 kDa), found in the cytosol of cells, particularly of liver, kidney, and intestine. They have a high content of cysteine and can bind copper, zinc, cadmium, and mercury. The SH groups of cysteine are involved in binding the metals. Acute intake (eg, by injection) of copper and of certain other metals increases the amount (induction) of these proteins in tissues, as does administration of certain hormones or cytokines. These proteins may function to store the above metals in a nontoxic form and are involved in their overall metaboHsm in the body. Sequestration of copper also diminishes the amount of this metal available to generate free radicals. 

A considerable amount of the gold that accumulates in the kidneys and liver of mammalian species is bound to MTs. This buildup of gold in the kidneys is accompanied by elevated levels of renal copper to form copper-rich, gold-bearing MTs. In cell lines that overproduce MT, there is commonly a resistance to the cytotoxic effects of gold compounds. This resistance is also seen often in parent lines that have been repeatedly exposed to gold complexes. The mechanisms of resistance include but are not limited to enhanced biosynthesis of MT [102]. 

Mogilnicka, E.M. and Webb, M. (1981) Comparative studies on the distribution of gold, copper and zinc in the livers and kidneys of rats and hamsters after treatment with sodium gold-195-labeled-aurofhiomalate. Journal of Applied Toxicology, 1, 287—291. 

In birds, copper concentrations in kidneys of the willow ptarmigan (Lagopus lagopus) are positively correlated with concentrations of cadmium (Wren et al. 1994). 

Maximum concentrations of copper in elasmobranchs and teleosts from all collection sites range from 7 to 15 mg/kg DW in eyeballs, intestines, muscle, scales, vertebrae, heart, and gonads and from 16 to 48 mg/kg DW in gills, kidneys, skin, and spleens. They reach 53 mg/kg DW in whole animals, 155 mg/kg DW in stomach contents, 208 mg/kg DW in feces, and 245 mg/kg DW in livers (Table 3.3). 

Marine mammals usually contain less than 44 mg Cu/kg DW in all tissues except livers. Copper in livers seldom exceeds 116 mg/kg DW except in polar bears (146 mg/kg DW), and manatees, Trichechus manatus, (1200 mg/kg DW) from a copper-contaminated site (Table 3.3). Maximum copper concentrations in terrestrial mammals from all collection sites are usually less than 29 mg/kg DW in all tissues except kidneys (108 mg/kg DW) and livers (1078 mg/kg DW Table 3.3). 

Liver, gall bladder, kidney Shorebirds Chile November 1981-March 1982 near abandoned copper mine liver vs. stomach contents 11-15 DW 137... 

Impalas (Aepyceros melampus) found dead in Kruger National Park, South Africa, had elevated concentrations of copper in livers (maximum 444 mg/kg FW) and kidneys (maximum 141 mg/kg FW) authors assert that copper poisoning is the most likely cause of death (Gummow et al. 1991), but this needs verification. Copper concentrations in bones, kidneys, and livers of white-tailed deer (Odocoileus virginianus) near a copper smelter and from distant sites are about the same. However, deer near the smelter have significantly elevated concentrations of cadmium in kidneys and livers, lead in bone, and zinc in kidneys (Storm et al. 1994). 

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