Copper Deficiency Effects

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). 

Copper deficiency effects are reported in mink (Mustela vison) and domestic swine. Copper deficiency in mink, as judged by reduced survival, occurs by feeding rations containing the equivalent of 3.5 mg Cu/kg BW daily for a period of 50 weeks (ATSDR 1990). Swine, which seem to have higher copper requirements than mink, given low copper diets equivalent to 15 to 36 mg Cu/kg B W daily for 7 days have decreased hemoglobin, hematocrit, and growth rate (ATSDR 1990). 

Data are scarce or missing on copper deficiency effects in aquatic flora and fauna and in avian and terrestrial mammalian wildlife additional studies of copper deficiency in these groups are merited. In sensitive terrestrial agricultural crops, copper deficiency occurs at less than 1.6 mg... 

Copper is an essential component of numerous key metalloenzymes which are critical in melanin formation, myelin formation and crosslinking of collagen and elastin. Copper plays a vital role in hemopoiesis, maintenance of vascular and skeletal integrity, and structure and function of the nervous system. Thus a deficiency of copper can lead to a variety of adverse effects such as increased fragility in bones, aneurysm formation in arteries and a loss of lysyl oxidase activity in cartilage.54 57 Articles on copper also appear in Siget1, volumes 3 and 5, all of volumes 12 and 13, and volume 14,... 

In patients with Wilson s disease, penicillamine is rapidly attached to copper and, although higher doses are used, taste disturbances develop in a lower frequency, about 4% (SED-8, 536). It has been suggested that dysgeusia is related to deficiency of copper or zinc, but a strong connection between taste impairment and urinary copper excretion has not been demonstrated (118). Serum copper concentrations remained within normal limits and copper supplements were not effective in prevention (119). 

Genetic and nutritional studies have illustrated the essential nature of copper for normal brain function. Deficiency of copper during the foetal or neonatal period will have adverse effects both on the formation and the maintenance of myelin (Kuo et al., 2001 Lee et al., 2001 Sun et al., 2007 Takeda and Tamana, 2010). In addition, various brain lesions will occur in many brain regions, including the cerebral cortex, olfactory bulb, and corpus striamm. Vascular changes have also been observed. It is also of paramount importance that excessive amounts of copper do not occur in cells, due to redox mediated reactions such that its level within cells must be carefully controlled by regulated transport mechanisms. Copper serves as an essential cofactor for a variety of proteins involved in neurotransmitter synthesis, e.g. dopamine P-hydroxylase, which transforms dopamine to nor-adrenahne, as well as in neuroprotection via the Cu/Zn superoxide dismutase present in the cytosol. Excess free copper is however deleterious for cell metabolism, and therefore intracellular copper concentration is maintained at very low levels, perhaps as low as 10 M. Brain copper homeostasis is still not well understood. 

Sulfur has an antagonistic effect on several essential trace elements. Excessive amounts of sulfur can induce a secondary deficiency of copper (mainly in animals), cobalt and selenium. Ho vever, not only the sulfur amino acid cysteine but also sulfate eliminates the adverse effects of copper-, cobalt-or selenium-based toxicities (Baker and Czarnecki-Maulden 1987). Sulfate increases the urinary loss of selenate, but not of selenite this explains the assumption that there is a direct antagonism between sulfate and selenate (Schrauzer 1998). 

The effect of traces of copper on oat-seedlings, grown in a copper-deficient medium, is shown in Fig. 11.4. Plainly, too little copper is bad for growth, and so is too much. Until recognized as such, copper-deficiency was the cause of many a crop failure in the reclaimed areas of Holland and Denmark. Copper-deficiency in farm animals leads to anaemia, demyelination of the spinal cord, and loss of pigmentation. Excess of copper storage in the liver of sheep leads to haemolysis and death. Sheep, fed on a diet deficient in copper, lose the crimp in their wool. Because it is the crimp that makes fine wool saleable, this causes economic loss to farmers (see Fig. 11.2). 

In 1968 the Monsanto Company announced the availability of novel soluble low molecular weight polyphenylene resins. These may be used to impregnate asbestos or carbon fibre and then cross-linked to produce heat-resistant laminates. The basic patent (BP 1037111) indicates that these resins are prepared by heating aromatic sulphonyl halides (e.g. benzene-1,3-disulphonyl dichloride) with aromatic compounds having replaceable nuclear hydrogen (e.g. bisphenoxy-benzenes, sexiphenyl and diphenyl ether). Copper halides are effective catalysts. The molecular weight is limited initially by a deficiency in one component. This is added later with further catalyst to cure the polymer. 

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