Copper deficiency, diseases

The cytochrome oxidase activity of liver, heart, and bone marrow is greatly reduced under conditions of copper deficiency. The catalase activity of liver and kidney is also decreased, but that of the heart is increased. On the other hand, Marston and his colleagues could find no such decrease in the cytochrome oxidase status of the tissues of copper deficient sheep. Much further study of this type is needed for the larger animals, particularly in relation to the naturally occurring copper-deficiency diseases of sheep and cattle. Only in this way does it seem likely that the different functional disturbances which occur in these animals, in addition to anemia, will be explained. 

Copper-deficiency diseases of grazing sheep and cattle have been shown to occur in various parts of the world. The history of their discovery and details of the conditions under which they occur have been given in detail by Russell up to 1944 and will not be presented here. In general, three main lines of evidence have served to establish copper deficiency as the cause of the maladies (1) sheep and cattle fail to thrive in certain areas, and anemia and specific symptoms of disease occur, all of which are overcome by copper supplements (2) the liver and blood of affected stock contain subnormal amounts of copper and (3) the herbage on which the stock graze, and in most cases the soils on which the herbage grows, contain subnormal amounts of copper. 

Chromium has proved effective in counteracting the deleterious effects of cadmium in rats and of vanadium in chickens. High mortality rates and testicular atrophy occurred in rats subjected to an intraperitoneal injection of cadmium salts however, pretreatment with chromium ameliorated these effects (Stacey et al. 1983). The Cr-Cd relationship is not simple. In some cases, cadmium is known to suppress adverse effects induced in Chinese hamster (Cricetus spp.) ovary cells by Cr (Shimada et al. 1998). In southwestern Sweden, there was an 80% decline in chromium burdens in liver of the moose (Alces alces) between 1982 and 1992 from 0.21 to 0.07 mg Cr/kg FW (Frank et al. 1994). During this same period in this locale, moose experienced an unknown disease caused by a secondary copper deficiency due to elevated molybdenum levels as well as chromium deficiency and trace element imbalance (Frank et al. 1994). In chickens (Gallus sp.), 10 mg/kg of dietary chromium counteracted adverse effects on albumin metabolism and egg shell quality induced by 10 mg/kg of vanadium salts (Jensen and Maurice 1980). Additional research on the beneficial aspects of chromium in living resources appears warranted, especially where the organism is subjected to complex mixtures containing chromium and other potentially toxic heavy metals. 

Two inherited human diseases that represent abnormal copper metabolism are Menkes syndrome and Wilson s disease. Menkes syndrome, with symptoms similar to those of copper deficiency, is characterized by a progressive brain disease, abnormally low copper concentrations in liver and other tissues, and diminished ability to transfer copper across the absorptive cells of the intestinal mucosa (USEPA 1980 Aaseth and Norseth 1986). Wilson s disease (hepatolenticular degeneration) is the only significant example of copper toxicity in humans. Wilson s disease is an autosomal recessive disorder that affects normal copper homeostasis and is characterized by excessive... 

Hair Camels with sway disease (severe copper deficiency) Nonpregnant females 6.4 DW 95... 

Strain genetically deficient in copper (Menkes disease) given subcutaneous injections of 50 pg copper chloride (CuCI2) on postnatal days 7 and 10. Before therapy, liver copper concentration was 3.1 mg/kg FW (vs. 30.1 mg/kg FW in normal mice)... 

Humans given zinc supplements should be aware of possible complications (Fosmire 1990). Low intakes of 100 to 300 mg of zinc daily in excess of the recommended dietary allowance of 15 mg Zn daily may produce induced copper deficiency, impaired immune function, and disrupted blood lipid profiles. Patients treated with zinc supplements (150 mg daily) to control sickle cell anemia and nonresponsive celiac disease developed a severe copper deficiency in 13 to 23 months normal copper status was restored by cessation of zinc supplements and increased dietary copper (Fosmire 1990). 

The first indications of interaction between copper and molybdenum came more than 40 years ago from studies of grazing cattle in certain areas of England. Afflicted animals lost weight, developed severe diarrhea, and (in extreme cases) died. The disease is sometimes called teart (rhymes with heart) or molybdenosis, and is caused by eating herbage rich in molybdenum (i.e., 20 to 100 mg/kg dry weight diet compared to <5 mg/kg in nearby healthy pastures) and low or deficient in copper and inorganic sulfate (Underwood 1979). Molybdenosis is a copper deficiency... 

The amino acid histidine is used for the treatment of copper overload in Wilson s disease and forms a strong 1 2 complex (Fig. 27) (553). Copper-histidine therapy is also an efficient treatment for copper deficiency in Menkes disease (554). 

Menkes disease Deficient cross-linking secondary to functional copper deficiency Depigmented (steely) hair Arterial tortuosity, rupture Cerebral degeneration Osteoporosis, anemia... 

Large amounts of copper are found in the liver, larger amounts in young individuals than in old. In cases of copper deficiency, anemia, hair discoloration, and other pathological symptoms have been observed. Increased levels of copper, which result from defense mechanism actions of the immune system, have been reported in infectious and cancer diseases (Sarkar, 1995). 

Zinc in Plant and Animal Nutrition. In 1854 A. Braun discovered the presence of zinc in plants and m 1869 J. Raulin proved diat it is essential for the growth of Aspergillus (153, 154). Its important role in die nutrition of many plants and animals has been demonstrated repeatedly (104, 105). When some pecan tines growing on a copper-deficient soil were treated widi a copper solution, die only trees which responded favorably were those treated with a solution which had been stirred up in a galvanized bucket and therefore contained zinc unintentionally (106). Zinc solutions are now used in the treatment of pecan rosette and other zinc-deficiency diseases of fruit trees and nut-bearing trees in the western states (112). 

Copper deficiency in plants is most frequent on organic soils, such as newly drained bogs, and on very sandy soils The severe copper deficiency often found when bogs and marshes are first used for crop production is called nyUinutliori disease in some parts of the world. 

Monugasiric animals, including humans, are less sensitive than ruminants to either copper deficiency or toxicity. Copper deficiency in people has been round only when other complications, such as excessive bleeding, general starvation, and iron deficiency, arc also present. Wilson s disease, an inherited disease ol humans, prevents the loss of excess copper tram the body and brings on copper toxicity. No direct relationships have been found between levels of avaitable copper in the soil and the copper status of humans. 

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