Copper is mainly absorbed through the gastrointestinal tract, but it can also be inhalated and absorbed dermally. It passes through the basolateral membrane, possibly via regulatory copper transporters, and is transported to the liver and kidney bound to serum albumin. The liver is the critical organ for copper homoeostasis. In the liver and other tissues, copper is stored bound to metallothionein, amino acids, and in association with copper-dependent enzymes, then partitioned for excretion through the bile or incorporation into intra- and extracellular proteins. The transport of copper to the peripheral tissues is accomplished through the plasma attached to serum albumin, ceruloplasmin or low-molecular-weight complexes. Copper may induce the production of metallothionein and ceruloplasmin. The membrane-bound copper transporting adenosine triphosphatase (Cu-ATPase) transports copper ions into and out of cells. Physiologically normal levels of copper in the body are held constant by alterations in the rate and amount of copper absorption, compartmental distribution, and excretion. (L277, L279)
For healthy, non-occupationally-exposed humans the major route of exposure to copper is oral. The mean daily dietary intake of copper in adults ranges between 0.9 and 2.2 mg. ... In some cases, drinking water may make a substantial additional contribution to the total daily intake of copper, particularly in households where corrosive waters have stood in copper pipes. ... All other intakes of copper (inhalation and dermal) are insignificant in comparison to the oral route. Inhalation adds 0.3-2.0 ug/day from dusts and smoke. Women using copper IUDs are exposed to only 80ug or less of copper per day from this source. The homeostasis of copper involves the dual essentiality and toxicity of the element. Its essentiality arises from its specific incorporation into a large number of proteins for catalytic and structural purposes. The cellular pathways of uptake, incorporation into protein and export of copper are conserved in mammals and modulated by the metal itself. Copper is mainly absorbed through the gastrointestinal tract. From 20 to 60% of the dietary copper is absorbed, with the rest being excreted through the feces. Once the metal passes through the basolateral membrane it is transported to the liver bound to serum albumin. The liver is the critical organ for copper homeostatis. The copper is partitioned for excretion through the bile or incorporation into intra- and extracellular proteins. The primary route of excretion is through the bile. The transport of copper to the peripheral tissues is accomplished through the plasma attached to serum albumin, ceruloplasmin or low-molecular weight complexes. ... The biochemical toxicity of copper, when it exceeds homeostatic control, is derived from its effects on the structure and function of biomolecules, such as DNA, membranes and proteins directly or through oxygen-radical mechanisms. The toxicity of a single oral dose of copper varies widely between species. ... The major soluble salts (copper(II) sulfate, copper(II) chloride) are generally more toxic than the less soluble salts (copper(II) hydroxide, copper (II) oxide). Death is preceded by gastric hemorrhage, tachycardia, hypotension, hemolytic crisis, convulsions and paralysis. ... Long-term exposure in rats and mice showed no overt signs of toxicity other than a dose-related reduction in growth after ingestion ... The effects included inflammation of the liver and degeneration of kidney tubule epithelium. ... Some testicular degeneration and reduced neonatal body and organ weights were seen in rats ... and fetotoxic effects and malformations were seen at high dose levels. ... Neurochemical changes have been reported after oral administration ... A limited number of immunotoxicity studies showed humoral and cell-mediated immune function impairment in mice after oral intakes in drinking-water ... Copper is an essential element and adverse health effects /in humans/ are related to deficiency as well as excess. Copper deficiency is associated with anemia, neutropenia and bone abnormalities but clinically evident deficiency is relatively infrequent in humans. .. Except for occasional acute incidents of copper poisoning, few effects are noted in normal /human/ populations. Effects of single exposure following suicidal or accidental oral exposure have been reported as metallic taste, epigastric pain, headache, nausea, dizziness, vomiting and diarrhea, tachycardia, respiratory difficulty, hemolytic anemia, hematuria, massive gastrointestinal bleeding, liver and kidney failure, and death. Gastrointestinal effects have also resulted from single and repeated ingestion of drinking-water containing high copper concentrations, and liver failure has been reported following chronic ingestion of copper. Dermal exposure has not been associated with systemic toxicity but copper may induce allergic responses in sensitive individuals. Metal fume fever from inhalation of high concentrations in the air in occupational settings have been reported ... A number of groups are described where apparent disorders in copper homeostasis result in greater sensitivity to copper deficit or excess than the general population. Some disorders have a well-defined genetic basis. These include Menkes disease, a generally fatal manifestation of copper deficiency; Wilson disease (hepatolenticular degeneration), a condition leading to progressive accumulation of copper; and hereditary aceruloplasminemia, with clinical symptoms of copper overload. Indian childhood cirrhosis and idiopathic copper toxicosis are conditions related to excess copper which may be associated with genetically based copper sensitivity ... These are fatal conditions in early childhood where copper accumulates in the liver. ... Other groups potentially sensitive to copper excess are hemodialysis patients and subjects with chronic liver disease. Groups at risk of copper deficiency include infants (particularly low birth weight/preterm babies, children recovering from malnutrition, and babies fed exclusively with cow's milk), people with maladsorption syndrome (e.g., celiac disease, sprue, cystic fibrosis), and patients on total parenteral nutrition. Copper deficiency has been implicated in the pathogenesis of cardiovascular disease. The adverse effects of copper must be balanced against its essentiality. Copper is an essential element for all biota ... At least 12 major proteins require copper as an integral part of their structure. It is essential for the utilization of iron in the formation of hemoglobin, and most crustaceans and molluscs possess the copper-containing hemocyanin as their main oxygen-carrying blood protein. ... A critical factor in assessing the hazard of copper is its bioavailablity. Adsorption of copper to particles and complexation by organic matter can greatly limit the degree to which copper will be accumulated ... At many sites, physiochemical factors limiting bioavailability will warrant higher copper limits. ...
Excess copper is sequestered within hepatocyte lysosomes, where it is complexed with metallothionein. Copper hepatotoxicity is believed to occur when the lysosomes become saturated and copper accumulates in the nucleus, causing nuclear damage. This damage is possibly a result of oxidative damage, including lipid peroxidation. Copper inhibits the sulfhydryl group enzymes such as glucose-6-phosphate 1-dehydrogenase, glutathione reductase, and paraoxonases, which protect the cell from free oxygen radicals. It also influences gene expression and is a co-factor for oxidative enzymes such as cytochrome C oxidase and lysyl oxidase. In addition, the oxidative stress induced by copper is thought to activate acid sphingomyelinase, which lead to the production of ceramide, an apoptotic signal, as well as cause hemolytic anemia. Copper-induced emesis results from stimulation of the vagus nerve. (L277, T49, A174, L280)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
致癌物分类
对人类无致癌性（未列入国际癌症研究机构IARC清单）。
No indication of carcinogenicity to humans (not listed by IARC).
People must absorb small amounts of copper every day because copper is essential for good health, however, high levels of copper can be harmful. Very-high doses of copper can cause damage to your liver and kidneys, and can even cause death. Copper may induce allergic responses in sensitive individuals. (L278, L279)
来源:Toxin and Toxin Target Database (T3DB)
毒理性
暴露途径
吸入，皮肤和/或眼睛接触
inhalation, skin and/or eye contact
来源:The National Institute for Occupational Safety and Health (NIOSH)
The pulmonary uptake of copper oxide /occurred/ in rats exposed to aerosols containing 50-80 mg/cu m. Animals were exposed for 15, 30, 45, or 60 minutes and killed immediately. Another group was exposed for 180 minutes and killed at 0, 3, 6, 12, 18, or 24 hours after exposure. Electron microscopic histologic examination showed that absorption of copper had occurred in animals exposed for 180 minutes. Copper oxide particles penetrated the epithelial cells of alveoli and were found in plasma 6 hours after exposure began. Copper oxide was also observed in the proximal convoluted tubules of the kidney. /Copper oxide/
VET: COPPER SOURCE. 80% COPPER CONTENT. LOW ABSORPTION RATE & HIGH FECAL EXCRETION RATE IN CATTLE & SWINE FEEDING TRIALS. IN GENERAL MONOGASTRIC ANIMALS UTILIZE /CUPRIC OXIDE/ BETTER THAN RUMINANTS. POULTRY UTILIZATION IS SOMEWHERE BETWEEN THE TWO.
Cheviot ewes (mean live weight 50 kg) were given single doses of 0, 2.5, 5, 10, or 20 g cupric oxide particles in gelatin capsules while receiving a diet of marginal copper content based on pelleted oats. After 65 days, liver copper concentrations had increased curvilinearly in relation to dose and all ewes given 10 or 20 g cupric oxide particles showed increases of at least 13.4 mmol/kg dry matter (850 ppm). Liver copper concentrations had generally declined after 85 days but biochemical and histological evidence of copper toxicity was recorded in one ewe which had received 20 g cupric oxide particles. Despite marked variations between individual sheep, a dose of 0.1 g/kg liveweight (5 g) was considered to be safe and did not induce clinical copper toxicity in five sheep of the susceptible North Ronaldsay breed given the same basal diet.
Crossbred steers, mean initial live weight 220 kg, were given a diet of barley and hay ad libitum. Each animal received a single oral does of 0, 5, 10, 20, or 40 g cupric oxide particles. A dose of 5 g cupric oxide particles increased liver copper stores for about 240 days and higher doses increased liver stores for longer but 40 g was no more effective than 20 g (85 mg/kg live weight). Variation among individuals was marked but the highest liver copper concentration recorded (7.59 mmol/kg dry matter) produced no biochemical evidence of copper toxicity. Cupric oxide particles were separated into three fractions, clumps, short rods and long; and 5 mg/kg live weight of each fraction given to steers of 173 kg mean live weight. The form of the particles did not affect either their retention in the alimentary tract or the accumulation of copper in the liver.
[EN] UNSYMMETRICAL SALTS, CCC-NHC PINCER METAL COMPLEXES, AND METHODS OF MAKING THE SAME [FR] SELS ASYMÉTRIQUES, COMPLEXES MÉTALLIQUES À PINCE CCC-NHC, ET LEURS PROCÉDÉS DE FABRICATION
Abstract Radiativelifetimes of several electronicstates of CuO have been determined by recording the exponential decay of the fluorescence following resonant excitation by a pulsed dye laser. The lifetimes extrapolated to zero pressure have been found to be 0.65 μsec for the A2Σ− state, 1.3 μsec for the C2Π state, 1.8 μsec for the D2Δ state, and more than 5 μsec for the A′ ( Ω = 1 2 ) state. In connection
Intriguing structural and magnetic properties correlation study on Fe<sup>3+</sup>-substituted calcium-copper-titanate
作者：P. R. Pansara、P. Y. Raval、N. H. Vasoya、S. N. Dolia、K. B. Modi
DOI：10.1039/c7cp06681c
日期：——
This communication presents a detailed study on a Fe3+ modified CaCu3Ti4O12 cubic perovskite system (CaCu3−xTi4−xFe2xO12 with x = 0.0–0.7) by performing X-ray powder diffractometry, DC SQUID magnetization and 57FeMössbauer spectroscopy. The first ever Mössbauerstudies on the system supported the reported peculiarity of the structure. Mössbauer analysis for the compositions x = 0.1, 0.3, and 0.5 suggest
本交流通过进行X射线粉末衍射法，对Fe 3+修饰的CaCu 3 Ti 4 O 12立方钙钛矿体系（CaCu 3- x Ti 4- x Fe 2 x O 12，x = 0.0-0.7）进行了详细研究， DC SQUID磁化强度和57 FeMössbauer光谱。Mössbauer对该系统进行的首次研究证明了该结构的独特性。组成x = 0.1、0.3和0.5的Mössbauer分析表明Fe 3+离子在两个不同的环境中。在八面体对称中，四极分裂较大的位点对应于Fe 3+，而在四面对称（A'-）构型中，化学位移和四极分裂较低的位点属于Fe 3+。随着Fe取代度的增加，Fe 3+似乎更倾向于A'-对称性。反铁磁特征保留到x = 0.3，但随着较高的Fe 3+取代，铁磁特征变弱。反铁磁行为向铁磁行为的转变与Fe 3+在占据Cu 2+的正方形平面对称结构中的优先占有有关。
Method of producing solution-derived metal oxide thin films
申请人：Sandia Corporation
公开号：US06086957A1
公开（公告）日：2000-07-11
A method of preparing metal oxide thin films by a solution method. A .beta.-metal .beta.-diketonate or carboxylate compound, where the metal is selected from groups 8, 9, 10, 11, and 12 of the Periodic Table, is solubilized in a strong Lewis base to form a homogeneous solution. This precursor solution forms within minutes and can be deposited on a substrate in a single layer or a multiple layers to form a metal oxide thin film. The substrate with the deposited thin film is heated to change the film from an amorphous phase to a ceramic metal oxide and cooled.
The present invention provides a composition comprising an amine oxide and an aqueous copper amine complex. Another embodiment of the present invention is a method for preserving and/or waterproofing a wood substrate by contacting the composition with the wood substrate. Yet another embodiment is an article comprising a wood substrate and the composition of the present invention. This composition has high efficacy against fungi, including copper tolerant fungi such as brown rot and soft rot, and is phase stable at high concentrations. Additionally, the amine oxide in the composition may impart waterproofing properties. The composition of the present invention is halide free and is environmentally friendly.
Disclosed herein are reusable composite materials for scavenging oxygen, methods of preparing the composite materials and method of using them. The composite materials contain porphyrin molecules and a metal oxide comprised within the porphyrin. The metal oxide is oxidizable in the presence of oxygen and the oxidation of the metal oxide is reversible upon exposure of the composite material to light of a fixed wavelength.
