In copper poisoning

Mechanisms implicated in copper poisoning include free radical production, alteration in activities of several enzymes, and interference with metallothionein synthesis. At the cellular level,... 

The specific treatment of WD is aimed at removing excessive body copper by chelation with D-penicillamine. Chelation therapy will reverse most of the clinical disturbances in the symptomatic WD patient, and will maintain nonsymptomatic WD patients in that state for their life-span (Marsden 1984, Mowet 1984). Patients who develop intolerance to D-penicillamine may be treated with equal success with Tri-entine (triethylene tetramine dihydrochloride) (Scheinberg 1991). Continuous oral zinc acetate therapy may also reduce the amount of excessive copper in the bloodstream (Brewer et al. 1983, Cossack 1987), but conclusive clinical tests on such a therapy have yet to be performed. Tetrathiomo-lybdate was successfully used to remove excessive copper in copper-poisoned sheep (Wing and Mehra 1990), and some clinical trials are currently in progress to ascertain the value of molybdenum in human WD therapy. It is pertinent to note here that in a case report on high molybdenum intake from a dietary supplement, an acute psychotic clinical picture was observed (Momci-lovic 1999). 

D-Penicillamine 11.26), similarly used in copper poisoning, is non-toxic. It is employed in Wilson s disease, an inherited error of metabolism in which dietary copper cannot be eliminated, but accumulates in brain, kidneys, and liver in such quantities that death occurs in the early years of life. Oral administration of penicillamine prevents this and can even reverse the pathological lesions produced by the copper ions. The copper—penicillamine complex is readily voided in the urine (Walshe, 1968). Penicillamine, being effective orally, is convenient to use in the later stages of treating chronic lead poisoning with intravenous EDTA. 

Metal metabolism The use of zinc in the treatment of copper deposition due to Wilson s disease was first proposed in the Netherlands by Schouwink in his 1961 PhD thesis [107, 108 ]. This was based on earher experience in veterinary medicine in Australia that zinc salts are effective in copper poisoning in sheep. Later observations showed that stimulation by zinc of metallothionein blocks the intestinal absorption of copper. Metallothionein binds both zinc and copper, but it has a higher affinity for the latter. It binds newly absorbed copper in enterocytes and prevents it from passing firom the gut into the circulation. Copper has no enterohepatic circulation, and Ihe shedding of enterocytes with copper still bound to metallothionein results in higher fecal copper excretion. 

The new data obtained on the elemental content of the ash from ritual censer confirm the hypothesis, which was postulated in earlier researches, about that possibility of the human copper-poisoning during the ritual narcotic inhalations. 

White phosphorus. This element burns in air and can produce severe thermal and chemical burns. It may reignite on drying. After washing, rapid but brief treatment with copper sulphate (to avoid systemic absorption and copper poisoning) is used to convert the phosphorus to copper phosphide which is then removed Hydrogen fluoride. This can form painful but delayed necrosis. Treat with calcium gluconate locally and monitoring of serum calcium levels, with administration of calcium where necessary... 

It is unclear whether long-term copper poisoning exists in humans. Some have related certain central nervous system disorders, such as giddiness, loss of appetite, excessive perspiration, and... 

In terrestrial vegetation, molybdenum and sulfur interfere with copper-induced deficiencies (Gupta 1979). Copper poisoning in cattle and other ruminants is governed by dietary concentrations of molybdenum and sulfate (Lewis et al. 1967 Todd 1969 Buckley and Tait 1981 Eisler 1989). Molybdenum and sulfur in mammalian diets cause a decrease in the availability of copper because of the formation of the biologically unavailable copper-thiomolybdate complex (Aaseth and Norseth 1986). Cattle die when grazing for extended periods on pastures where the ratio of copper to molybdenum... 

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). 

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). 

Chronic copper poisoning in domestic sheep is first characterized by a period of passive accumulation of copper in the tissues. This period varies from a few weeks to more than a year. During this time the animal appears outwardly normal although the liver may contain more than 1000 mg Cu/kg DW and plasma activities of aspartate transaminase, sorbitol dehydrogenase, lactic... 

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). 

Baker, J.T.P. 1969. Histological and electron microscopical observations on copper poisoning in the winter flounder (Pseudopleuronectes americanus). Jour. Fish. Res. Bd. Can. 26 2785-2793. 

Carbonell, G. and J.V. Tarazona. 1993. A proposed method to diagnose acute copper poisoning in cultured rainbow trout (Oncorhynchus mykiss). Sci. Total Environ., Suppl. 1993, Part 2 1329-1334. 

Higgins, R.J. 1981. Chronic copper poisoning in growing pigs. Veterin. Rec. 109(7) 134-135. 

MacPherson, A. and R.G. Hemingway. 1969. The relative merit of various blood analyses and liver function tests in giving an early diagnosis of chronic copper poisoning in sheep. Brit. Veterin. Jour. 125 213-221. 

Thompson, R.H. and J.R. Todd. 1974. Muscle damage in chronic copper poisoning of sheep. Res. Veterin. Sci. 16 97-99. 

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