Copper: deficiency

Copper is required for all forms of aerobic and most forms of anaerobic life. In humans, the biological function of copper is related to the enzymatic action of specific essential copper proteins (66). Lack of these copper enzymes is considered a primary factor in cerebral degeneration, depigmentation, and arterial changes. Because of the abundance of copper in most human diets, chemically significant copper deficiency is extremely rare (67). 

About 50% of copper in food is absorbed, usually under equitibrium conditions, and stored in the tiver and muscles. Excretion is mainly via the bile, and only a few percent of the absorbed amount is found in urine. The excretion of copper from the human body is influenced by molybdenum. A low molybdenum concentration in the diet causes a low excretion of copper, and a high intake results in a considerable increase in copper excretion (68). This copper—molybdenum relationship appears to correlate with copper deficiency symptoms in cattle. It has been suggested that, at the pH of the intestine, copper and molybdate ions react to form biologically unavailable copper molybdate (69). 

Plant and Animal Nutrient. Copper is one of seven micronutrients that has been identified as essential to the proper growth of plants (87). Cereal crops are by far the most affected by copper deficiency (see Wheat and other cereal grains). Greenhouse studies have shown yield increases from 38% to over 500% for wheat, barley, and oats (88) using copper supplementation. A tenfold increase in the yield of oats was reported in France (89). Symptoms of copper deficiency vary depending on species, but often it is accompanied by withering or chlorosis in the leaves that is not ammenable to iron supplementation. In high concentrations, particularly in low pH sods, copper can be toxic to plants. 

Research into elastin, its properties, and the fiber formation was for a considerable period of time hindered due to its insolubihty. However, discovery of the soluble tropoelastin precursor made new investigations possible. The tropoelastin protein can be isolated from copper-deficient animals. However, this is a very animal-unfriendly and low yielding process [2]. Therefore, it is preferred to obtain tropoelastin from overexpression in microbial hosts such as Escherichia coli (E. coli). Most studies are thus based on tropoelastin obtained via bacterial production. 

Extensive structural, optical, and electronic studies on the chalcopyrite semiconductors have been stimulated by the promising photovoltaic and photoelectrochem-ical properties of the copper-indium diselenide, CuInSe2, having a direct gap of about 1.0 eV, viz. close to optimal for terrestrial photovoltaics, and a high absorption coefficient which exceeds 10 cm . The physical properties of this and the other compounds of the family can be modulated to some extent by a slight deviation from stoichiometry. Thus, both anion and cation deficiencies may be tolerated, inducing, respectively, n- and p-type conductivities a p-type behavior would associate to either selenium excess or copper deficiency. 

Adachi, S., Takemoto, K., Hirosuc, T. and Hosogai, Y. (1993). Spontaneous and 2-nitropropane induced levels of 8-hydroxy-2 -deoxyguanosine in liver DNA of rats fed iron-deficient or manganese- and copper-deficient diets. Carcinogenesis 14, 265-268. 

D. Gries, S. Klatt, and M. Runge, Copper-deficiency-induced phytosidero-phore release in the calcicole grass Hordelymus europaeus. New. Phytol 140 95 (1998). 

Under conditions of copper deficiency, some methanotrophs can express a cytosolic, soluble form of MMO (sMMO) (20-23), the properties of which form the focus of the present review. The sMMO system comprises three separate protein components which have all been purified to homogeneity (24,25). The hydroxylase component, a 251 kD protein, contains two copies each of three subunits in an a 82y2 configuration. The a subunit of the hydroxylase houses the dinuclear iron center (26) responsible for dioxygen activation and for substrate hydroxylation (27). The 38.6 kD reductase contains flavin adenine dinucleotide (FAD) and Fe2S2 cofactors (28), which enable it to relay electrons from reduced nicotinamide adenine dinucleotide (NADH) to the diiron center in the... 

In addition to all of the expected enzyme systems present in leaf tissue, fresh tea leaves contain a high level of polyphenol oxidase that catalyzes the oxidation of the catechins by atmospheric oxygen. Tea polyphenol oxidase exists as series of copper-containing (0.32%) isoenzymes. The major component has a molecular weight of about 144,000.54 The enzyme is concentrated in the leaf epidermis.55 Soil copper deficiency is sometimes responsible for inadequate oxidation during processing.56... 

Loessial soils in the Loess Plateau contained 0.01-4.20 mg/kg DTPA-extractable Cu with an average of 0.93 mg/kg (Table 7.7). Bioavailable Cu in the North China Plain varied from 0.07-9.95 mg/kg. In the North West region, soils contained 0.06-19.20 mg/kg DTPA-extractable Cu. The average bioavailable Cu was 1.83 mg/kg in the calcareous paddy soils with a range of trace to 6.85 mg/kg. Copper deficiency was not often observed in the arid and semi-arid soils of China. 

Alberta Agriculture, Food and Rural Development (1999). Copper Deficiency Diagnosis and Correction, Agdex 532-3. 

Karamanos, R.E., Kruger, G.A. and Stewart, J.W.B. (1986). Copper deficiency in cereal and oilseed crops in Northern Canadian prairie soils , Agronomy Journal, 78, 317-323. 

The regulation of superoxide formation by SOD can affect both in vivo and ex vivo lipid peroxidation. Thus, SOD inhibited lipid peroxidation in cats following regional intestinal ischemia and reperfusion [33], Similarly, the treatment of rats with polyethylene glycol superoxide dismutase (PEG-SOD) prevented the development of lipid peroxidation in hepatic ischemia-reperfusion injury [34], Interesting data have been reported by Bartoli et al. [35]. They showed that SOD depletion in the liver of rats feeding with a copper-deficient diet... 

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. 

Frank, A., V. Galgan, and L.R. Petersson. 1994. Secondary copper deficiency, chromium deficiency and trace element imbalance in the moose (Alces alces L.) effect of anthropogenic activity. Ambio 23 315-317. 

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... 

Adverse effects of copper deficiency can be documented in terrestrial plants and invertebrates, poultry, small laboratory animals, livestock — especially ruminants — and humans. Data are scarce or missing on copper deficiency effects in aquatic plants and animals and in avian and mammalian wildlife. Copper deficiency in sheep, the most sensitive ruminant mammal, is associated with depressed growth, bone disorders, depigmentation of hair or wool, abnormal wool growth, fetal death and resorption, depressed estrous, heart failure, cardiovascular defects, gastrointestinal disturbances, swayback, pathologic lesions, and degeneration of the motor tracts of the spinal cord (NAS 1977). 

Increased yields of various crops occur when copper salts are added to fertilizers at 300 to 800 mg Cu/m3 (NAS 1977). In com (Zea mays) and other vegetables, younger plants are more sensitive to copper deficiency than mature plants in all cases, copper-deficient vegetables show chlorosis, reduced growth and reproduction, and low survival (Gupta 1979). 

No evidence of copper deficiency exists in terrestrial species of invertebrates examined. However, relatively low concentrations of copper stimulated growth and reproduction. Reproduction in mites (Platynothrus peltifer) increases when fed diets containing 28 mg Cu/kg DW (vs. 13 mg/kg in controls) for 3 months (Denneman and van Straalen 1991). Also, juveniles of earthworms (Eisenia andrei) show increased growth at 18 mg Cu/kg DW soil after 12 weeks (van Gestel et al. 1991). 

No documented report of fatal copper deficiency is available for any species of aquatic organism, and no correlation is evident in aquatic biota for the presumed nutritional copper requirements of a species and its sensitivity to dissolved copper (Neff and Anderson 1977). Extremely low copper concentrations (5.5 and 6.7 mg/kg DW) in whole bodies of 2 of 17 species of crustaceans from the Antarctic Ocean support the hypothesis that certain Antarctic species may show copper deficiencies or reduced metal requirements (Petri and Zauke 1993). 

Copper deficiency in humans and other mammals is characterized by slow growth, hair loss, anemia, weight loss, emaciation, edema, altered ratios of dietary copper to molybdenum and other metals, impaired immune response, decreased cytochrome oxidase activity, central nervous system histopathology, decreased phospholipid synthesis, fetal absorption, and eventually death (NAS 1977 Gallagher 1979 Kirchgessner et al. 1979 USEPA 1980 ATSDR 1990 Percival 1995). 

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