Maximum blood copper levels were observed within 1 to 3 hours following oral administration, and about 50 percent of ingested copper was absorbed. Copper absorption is believed to occur by two mechanisms, one energy- dependent and the other enzymatic. Factors that can interfere with copper absorption include competition for binding sites with zinc, interactions with molybdenum and sulfates, chelation with phytates, and inhibition by ascorbic acid. Copper absorbed from the intestine is transported quickly into blood serum and deposited in the liver bound to metallothionein. It is released and incorporated into ceruloplasmin, a copper-specific transport protein. The remaining copper in the serum binds to albumin or amino acids or is contained in the erythrocytes. About 80 percent of the absorbed copper is bound to liver metallothionein; the remainder is included into cytochrome c oxidase or sequestered by lysosomes.
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
对人类不具有致癌性（未被国际癌症研究机构IARC列名）。
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
该物质可以通过吸入其气溶胶和通过吞食被吸收进人体。
The substance can be absorbed into the body by inhalation of its aerosol and by ingestion.
来源:ILO-WHO International Chemical Safety Cards (ICSCs)
Primarily absorbed in the small intestine. Based on studies with radioactive isotopes of copper, most copper is absorbed from the stomach and duodenum of the gastrointestinal tract. Maximum blood copper levels are observed within 1 to 3 hours following oral administration, and about 50 percent of ingested copper was absorbed. Copper absorption is proposed to occur by two mechanisms, one energy- dependent and the other enzymatic. Factors that can interfere with copper absorption include competition for binding sites with zinc, interactions with molybdenum and sulfates, chelation with phytates, and inhibition by ascorbic acid (vitamin C). Copper absorbed from the gastrointestinal tract is transported rapidly to blood serum and deposited in the liver bound to metallothionein. From 20 to 60% of the dietary copper is absorbed.
This drug is 80% eliminated via the liver in bile. Minimal excretion by the kidney. Metabolism studies show that persons with daily intakes of 2-5 mg of copper per day absorbed 0.6 to 1.6 mg (32%), excreted 0.5 to 1.3 mg in the bile, passed 0.1 to 0.3 mg directly into the bowel, and excreted 0.01 to 0.06 mg in the urine. As the data indicate, urinary excretion plays a negligible role in copper clearance, and the main route of excretion is in the bile. Other nonsignificant excretory routes include saliva, sweat, menstrual flow, and excretion into the intestine from the blood.
The body of a 70 kg healthy individual contains approximately 110 mg of copper, 50% of which is found in the bones and muscles, 15% in the skin, 15% in the bone marrow, 10% in the hepatic system, and 8% in the brain. The distribution of copper is affected by sex, age, and the amount of copper in the diet. Brain and liver have the highest tissue levels (about one-third of the total body burden), with lesser concentrations found in the heart, spleen, kidneys, and blood. The iris and choroid of the eye have very high copper levels. Erythrocyte copper levels are generally stable, however, plasma levels fluctuate widely in association with the synthesis and release of ceruloplasmin. Plasma copper levels during gestation may be 2-3 times levels measured before pregnancy, due to the increased synthesis of ceruloplasmin.
Effect of hydrogen ion (H+) concentration, water hardness, suspended solids, fish age, size, and species, acclimatization to copper, and levels of copper in food on poisoning of fish by copper sulfate used as a herbicide in freshwater ponds is discussed. Copper levels in muscle, kidney, and organs of rainbow trout were approximately 0.8-1.1, 2.0-2.3, and 115-150 mg/kg fresh weight, respectively, after 12 months intermittent exposure to various copper sulfate containing formulations 0.6, 2.0, and 100 mg/kg, respectively, in controls ... .
Male rats were orally administered for 2, 5, and 11 days with 0.5 mmol/kg of copper cmpd. ... In the case of cupric carbonate, copper was much more distributed in the tissues, especially in the liver, than for copper sulfate. The copper level increased progresively in mitochondria lysosomal fractions of the liver in proportion to the period of administration. In the 105,000 g supernatant fraction, copper was distributed in the metallothionein fraction rather than in the superoxide dismutase fraction. The administration of copper cmpd resulted in an increase in the zinc level in the liver, kidney and spleen, preferentially in the metallothionein fraction of the liver, but it seemed to have little effect on iron metabolism.
The limiting current density is increased without detrimentally affecting the quality of the metal deposit in an electrolytic process employing an electrolyte containing a dissolved metal sulfate, by adding sufficient quantities of the metal sulfate in a particulate state to maintain a solids concentration of the metal sulfate in the electrolyte during the electrodeposition.
Aqueous solutions containing dithionic acid and/or metal dithionate
申请人：——
公开号：US20020002128A1
公开（公告）日：2002-01-03
This invention relates to solutions of dithionic acid and/or dithionate salts for use in metal finishing processes such as those used for the cleaning, activating, electroplating, electroless plating, conversion coating and/or other pre-treatment or post-treatment of a metallic surface. In particular the solutions are a useful electrolyte for the electroplating of metallic coatings, especially, Sn, Cu, Ni, Zn and precious metals, onto metal or plastic substrates and/or other surfaces.
Aqueous solutions containing dithionic acid and /or metal dithionate for metal finishing
申请人：——
公开号：US20040082489A1
公开（公告）日：2004-04-29
This invention relates to solutions of dithionic acid and/or dithionate salts which use in metal finishing processes such those used for the cleaning, activating, electroplating, electroless plating, conversion coating and/or other pre-treatment or post-treatment of a metallic surface. In particular the solutions are a useful electrolyte for the electroplating of metallic coatings, especially, Sn, Cu, Ni, Zn and precious metals, onto metal or plastic substrates and/or other surfaces.
Novel substituted triazolo[1,5-a]pyrimidine-2-sulfonamides, e.g., 5,7-dimethyl-N-(2,6-dichlorophenyl)-1,2,4-triazolo[1,5-a]pyrimidine-2-sulf onamide and their agriculturally acceptable salt are prepared. These compounds and compositions containing them are useful for the control of unwanted vegetation. Novel substituted triazolo[1,5-a]pyrimidine-2-sulfonyl chlorides and substituted anilines and their use as intermediates are also described.
Novel substituted 1,2,4-triazolo[1,5-a]pyrimidine-2-sulfonamides and
申请人：The Dow Chemical Company
公开号：US04755212A1
公开（公告）日：1988-07-05
Novel compounds, e.g., 5,7-dimethyl-N-(2,6-dichlorolphenyl)-1,2,4-triazolo[1,5-a]pyrimidine-2-sul fonamide and their compositions and use in the control of weeds and in the suppression of nitrification of ammonium nitrogen in soil. Other novel compounds and their compositions and use in the inhibition of bolting in sugar beets. Other novel compounds and their compositions and use as plant gametocides.
