Copper Sulfate
Daten werden ergänzt – lade die Seite später neu, um den aktuellen Stand zu sehen
10124-44-4O=S(=O)([O-])[O-].[Cu+2]ARUVKPQLZAKDPS-UHFFFAOYSA-LCupric sulfate appears as a white or off-white solid. Melting point 200 °C with decomposition. Non-combustible.
10124-44-4、18939-61-2、7758-98-7DTXSID6034479CHEMBL604CHEBI:23414Plastics -> N.a.
Plastics -> Pigments agents
2.29 at 59 °F (USCG, 1999) - Denser than water; will sink
3.6
3.6 g/cm³
3.6 @25 °C
Grayish-white to greenish-white rhombic crystals or amorphous powder /SRP: somewhat wet/
White when dehydrated
Gray to white and has rhombic crystals
Very soluble in hot water, soluble cold water
Sicherheitsangaben dienen nur zur Orientierung und ersetzen weder das Sicherheitsdatenblatt (SDB) des Lieferanten noch geltende Vorschriften oder eine fachliche Bewertung.
Warning
H302: Harmful if swallowed [Warning Acute toxicity, oral]
P264, P264+P265, P270, P273, P280, P301+P317, P302+P352, P305+P351+P338, P321, P330, P332+P317, P337+P317, P362+P364, P391, and P501 (click each P-code to see the statement)
This chemical does not meet GHS hazard criteria for 1.1% (14 of 1268) of reports.
Danger
H302 (96.3%): Harmful if swallowed [Warning Acute toxicity, oral]
Chemical: Sulfuric acid, copper(2+) salt (1:1)
Commission Regulation No 844/2012
Sulfuric acid copper(2+) salt (1:1) is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Sulfuric acid copper(2+) salt (1:1) are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)
REACH registered substance: Copper sulphate (EC: 231-847-6)
Sulfuric acid, copper(2+) salt: Does not have an individual approval but may be used as a component in a product covered by a group standard. It is not approved for use as a chemical in its own right.
Copper sulphate: Does not have an individual approval but may be used under an appropriate group standard
Excerpt from ERG Guide 151 [Substances - Toxic (Non-Combustible)]:
Not combustible. Gives off irritating or toxic fumes (or gases) in a fire. Many reactions may cause fire or explosion. See Chemical dangers
V - Various
QV - Various
About 80 percent of the absorbed copper is bound to liver metallothionein; the remainder is incorporated into cytochrome c oxidase or sequestered by lysosomes. The bioavailability of copper from the diet is about 65-70% depending on a variety of factors including chemical form, interaction with other metals, and dietary components.
Copper is an essential mineral that plays a key role in many physiological processes, including angiogenesis, skin generation and expression and stabilization of skin proteins. Copper is found naturally in many food sources including meats, vegetables, and grains. Copper has potent biocidal properties and is used to eliminate bacteria, viruses and parasites,. Copper is one of the nine essential minerals for humans, as it plays an imperative role in various physiological pathways in basically all human tissue, as well as in the health of the dermis and epidermis. In addition to the above, copper is essential in wound healing, as it promotes angiogenesis and skin extracellular matrix formation and stabilization.
This drug is an essential trace element for the functioning of many metalloenzymes including ceruloplasmin, ferroxidase II, lysyl oxidase, monoamine oxidase, Zn-copper superoxide dismutase, tyrosinase, dopamine-β-hydroxylase, and cytochrome-c-oxidase. It is involved in erythropoiesis & leukopoiesis, bone mineralization, elastin and collagen cross-linking, oxidative phosphorylation, catecholamine metabolism, melanin formation & antioxidant protection of cells. Cupric sulfate may also have a role in iron turnover, ascorbic acid metabolism, phospholipid metabolism, myelin formation, glucose homeostasis, and cellular immune defense. After the metal passes through the basolateral membrane it is transported to the liver, attached to serum albumin. The liver is the critical organ for the homeostasis of copper. The copper is then prepared for excretion through the bile or incorporation into various proteins. The transport of copper to the peripheral tissues is accomplished through the plasma attached to serum albumin, ceruloplasmin or low-molecular-weight complexes. In the dermis, copper promotes dermal fibroblasts proliferation, upregulates collagen (types I, II, and V) and elastin fiber components (elastin, fibrillins) production by fibroblasts, through the induction of TGF-β, promotes heat shock protein-47, important for collagen fibril formation, serves as a cofactor of LOX enzyme required for extracellular matrix protein cross-linking, stabilizes the skin ECM once formed, as increased crosslinking of collagen and elastin matrices occurs in a copper dose dependant manner, serves as a cofactor of superoxide dismutase, an antioxidant enzyme in the skin, essential for protection against free radicals, inhibits cellular oxidative effects such as membrane damage and lipid peroxidation, acts as a cofactor of tyrosinase, a melanin biosynthesis essential enzyme responsible for skin and hair pigmentation. In reference to its role as a biocide, copper is an essential nutrient for many organisms. It acts as a cofactor in respiration, and therefore copper is required for aerobic metabolism. Accumulation of copper ions or intracellular release of free copper ions from proteins lead to cell damage. Copper catalyzes reactions that result in the production of hydroxyl radicals through the Fenton and Haber-Weiss reactions. The highly reactive oxygen intermediates lead to lipid peroxidation and oxidation of proteins. Free copper ions oxidize sulfhydryl groups, such as cysteine, in proteins or the cellular redox buffer glutathione. In particular, copper ions inactivate proteins by damaging Fe-S clusters in cytoplasmic hydratases.
Wird geladen…
Soluble in methanol (1.1 g/100 ml), but insoluble in ethanol; it readily dissolves in aqueous ammonia and excess alkali metal cyanides, with the formation of complexes
In water, 243 g/l @ 0 °C.
75.4 g/100 cc water @ 100 °C
1.04 g/100 cc methanol @ 18 °C
Solubility in water, g/l at 20 °C: 203 (freely soluble)
FDA approved drugs -> Active ingredient
FDA approved drugs -> Active ingredient
When heated to decomposition it emits toxic fumes of /sulfur oxides/.
650 °C (decomp to cupric oxide)
SLIGHT DECOMP ABOVE 200 °C
650 °C. This produces toxic fumes of sulfur oxides (see ICSC 0074). Reacts violently with hydroxylamine. This generates fire hazard. Reacts with magnesium powder. This produces flammable/explosive gas (hydrogen - see ICSC 0001). Reacts with acetylene and potassium chlorate. This generates explosion hazard. Attacks some metals in the presence of water.
INGESTION: copper sulfate may induce severe gastroenteric distress (vomiting, gastroenteric pain, and local corrosion and hemorrhages), prostration, anuria, hematuria, anemia, increase in white blood cells, icterus, coma, respiratory difficulties, and circulatory failure. (USCG, 1999)
A strong irritant; [Merck Index] A severe skin and eye irritant; A respiratory tract irritant; Can cause copper poisoning after ingestion; [ICSC] Interferes with embryo development in high-dose animal studies; [REPROTOX] An irritant; [MSDSonline] See Copper sulfate. See Copper.
In accordance with 21 CFR 184.1(b)(1), the ingredient is used in food with no limitation other than current good manufacturing practice. The affirmation of this ingredient as generally recognized as safe (GRAS) as a direct human food ingredient is based upon the following current good manufacturing practice conditions of use: 1) The ingredient is used as a nutrient supplement as defined in 21 CFR 170.3(o)(20) of this chapter and as a processing aid as defined in 21 CFR 170.3(o)(24) of this chapter. 2) The ingredient is used in food at levels not to exceed current good manufacturing practice. Copper sulfate may be used in infant formula in accordance with section 412(g) of the Federal Food, Drug, and Cosmetic Act (the act) or with regulations promulgated under section 412(a)(2) of the act. Prior sanctions for this ingredient different from the uses established in this section do not exist or have been waived.
Trace minerals added to animal feeds. These substances added to animal feeds as nutritional dietary supplements are generally recognized as safe when added are levels consistent with good feeding practice. Element: Copper; Source compound: copper sulfate. (All substances listed may be in anhydrous or hydrated form.)
A tolerance is established in potable water for residues of copper resulting from the use of the algicides or herbicides basic copper carbonate (malachite), copper sulfate, copper monoethanolamine, and copper triethanolamine to control aquatic plants in reservoirs, lakes, ponds, irrigation ditches, and other potential sources of potable water.
Anhydrous CUPRIC SULFATE serves as a weak oxidizing agent. Causes hydroxylamine to ignite. Gains water readily. The hydrated salt is vigorously reduced by hydroxylamine [Mellor 8:292(1946-1947)]. Both forms are incompatible with finely powdered metals. Both are incompatible with magnesium, corrode steel and iron, may react with alkalis, phosphates, acetylene gas, hydrazine, or nitromethane, and may react with beta-naphthol, propylene glycol, sulphathiazole and triethanolamine if the pH exceeds 7 (NTP, 1992). Both act as acidic salts, corrode metals and irritate tissues.
Cupric sulfate is designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance.
The solution in water is a weak acid. Decomposes at 650 °C. This produces toxic fumes of sulfur oxides (see ICSC 0074). Reacts violently with hydroxylamine. This generates fire hazard. Reacts with magnesium powder. This produces flammable/explosive gas (hydrogen - see ICSC 0001). Reacts with acetylene and potassium chlorate. This generates explosion hazard. Attacks some metals in the presence of water.
Excerpt from ERG Guide 151 [Substances - Toxic (Non-Combustible)]:
In case of fire in the surroundings, use appropriate extinguishing media.
Fresh air, rest.
Rinse skin with plenty of water or shower. Refer for medical attention if skin irritation occurs.
First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.
Do NOT induce vomiting. Give one or two glasses of water to drink. Refer for medical attention .
Environmental concerns - land spill: Dig a pit, lagoon,or holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./ Cover solids with a plastic sheet to prevent dissolving in rain or fire fighting water.
Environmental concerns - water spill: Neutralize with agricultural lime (CaO), crushed limestone (CaCO3), or sodium bicarbonate (NaHCO3). Adjust pH to neutral (pH= 7). Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates.
SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.
Group III Containers (both combustible and non-combustible) that previously held organic mercury, lead, cadmium, arsenic, or inorganic pesticides should be triple rinsed, punctured and disposed of in a sanitary landfill. Non-rinsed containers should be encapsulated and buried at a specially designated landfill site. /Organic mercury, lead, cadmium, arsenic, or inorganic pesticides/
The following wastewater treatment technologies have been investigated for copper (II) sulfate: activated carbon.
Add slowly to a large container of water. Stir in slight excess of soda ash. Let stand for 24 hr. Decant or siphon into another container and neutralize with 6 M HCl. ... The sludge may be added to landfill. Recommendable methods: Precipitation, solidification, & landfill. Peer-review: ... Copper can be recovered by cation exchange. (Peer-review conclusions of an IRPTC expert consultation (May 1985))
Personal protection: particulate filter respirator adapted to the airborne concentration of the substance, protective clothing, protective gloves and safety goggles. Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Then store and dispose of according to local regulations.
Personnel protection: Keep upwind. ... Avoid breathing vapors or dusts. Wash away any material which may have contacted the body with copious amounts of water or soap and water.
If material not involved in fire: Keep material out of water sources & sewers. Build dikes to contain flow as necessary.
SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants.
SRP: Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. Quality assurance to ascertain the completeness of the cleaning procedures should be implemented before the decontaminated protective clothing is returned for reuse by the workers.
EYES: irrigate opened eyes for several minutes under running water. INGESTION: do not induce vomiting. Rinse mouth with water (never give anything by mouth to an unconscious person). Seek immediate medical advice. SKIN: should be treated immediately by rinsing the affected parts in cold running water for at least 15 minutes, followed by thorough washing with soap and water. If necessary, the person should shower and change contaminated clothing and shoes, and then must seek medical attention. INHALATION: supply fresh air. If required provide artificial respiration.
THE IV INDUCED STIMULATION OF ALPHA-ADRENERGIC NERVOUS SYSTEM BY CUPRIC SULFATE WAS PARTIALLY ATTENUATED BY PRETREATMENT OF SHEEP WITH METHYSERGIDE. PHENOXYBENZAMINE COMPLETELY BLOCKED THE EFFECTS OF CUPRIC SULFATE & TREATMENT WITH PROPRANOLOL ENHANCED THE EFFECTS.
Acute copper (II) sulfate poisoning in the mouse induces renal tubular degeneration and necrosis. Administration of sodium 2,3-dimercaptopropane-sulfonate effectively prevented the development on the morphological sequelae of copper intoxication.
Pokeweed mitogen (PWM), a T cell-dependent polyclonal B cell activator, stimulates the differentiation of immunoglobin secreting cells from normal human peripheral blood mononuclear cells. ... Peripheral blood mononuclear cells failed to generate immunoglobin secreting cells in response to poke weed mitogen after brief exposure to D-penicillamine and copper sulfate; preincubation with either penicillamine or copper sulfate alone had no effect. Experiments utilizing purified populations of B and T cells indicated that penicillamine and copper sulfate markedly inhibited helper T cell activity but not B cell function.
Dimercaptosuccinic acid ... administered intragastrically to rabbits after sc administration of copper sulfate promoted urinary excretion.
For more Interactions (Complete) data for COPPER(II) SULFATE (10 total), please visit the HSDB record page.
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)
LC50 Anguilla rostrata (American eel) 3.20 mg/l/96 hr. /Conditions of bioassay not specified/
LC50 Schistosoma mansoni (Miricidia) 8.5 mg/l per hr. /Conditions of bioassay not specified/
LC90 Schistosoma mansoni (Miricidia) 15.75 mg/l per hr. /Conditions of bioassay not specified/
LC50 Puntius conchonius 0.709 mg/l/48 hr in water hardness of 310 mg/l calcium carbonate. /Static bioassay/
For more Ecotoxicity Values (Complete) data for COPPER(II) SULFATE (17 total), please visit the HSDB record page.
Terrestrial Fate: In soil, copper sulfate is partly washed down to lower levels, partly bound by soil components, and partly oxidatively transformed.
... Granular copper sulfate /was applied/ to the surface of Hoover Reservoir, Franklin County, Ohio. Soluble and particulate cupric copper concn at several depths were measured by atomic absorption spectrophotometry for four days after application. The soluble cupric copper concn decreased to near baseline values in 2 to 6 hr when 0.2 or 0.4 g of copper sulfate per square meter were added to the surface. Most of the copper sulfate was dissolved in the first 1.75 m of the water column, and only 2 percent of the total copper sulfate reached the depth of approx 4.5 m.
The substance can be absorbed into the body by inhalation of its aerosol and by ingestion.
Oral (L277) ; inhalation (L277) ; dermal (L277)
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. ...
Cough. Sore throat.
Redness. Pain.
Redness. Pain. Blurred vision.
Abdominal pain. Burning sensation. Nausea. Vomiting. Diarrhoea. Shock or collapse.
Breathing high levels of copper can cause irritation of the nose and throat. Ingesting high levels of copper can cause nausea, vomiting, diarrhea, headache, dizziness, and respiratory difficulty. (L278, L279)
In accordance with 21 CFR 184.1(b)(1), the ingredient is used in food with no limitation other than current good manufacturing practice. The affirmation of this ingredient as generally recognized as safe (GRAS) as a direct human food ingredient is based upon the following current good manufacturing practice conditions of use: 1) The ingredient is used as a nutrient supplement as defined in 21 CFR 170.3(o)(20) of this chapter and as a processing aid as defined in 21 CFR 170.3(o)(24) of this chapter. 2) The ingredient is used in food at levels not to exceed current good manufacturing practice. Copper sulfate may be used in infant formula in accordance with section 412(g) of the Federal Food, Drug, and Cosmetic Act (the act) or with regulations promulgated under section 412(a)(2) of the act. Prior sanctions for this ingredient different from the uses established in this section do not exist or have been waived.
Trace minerals added to animal feeds. These substances added to animal feeds as nutritional dietary supplements are generally recognized as safe when added are levels consistent with good feeding practice. Element: Copper; Source compound: copper sulfate. (All substances listed may be in anhydrous or hydrated form.)
A tolerance is established in potable water for residues of copper resulting from the use of the algicides or herbicides basic copper carbonate (malachite), copper sulfate, copper monoethanolamine, and copper triethanolamine to control aquatic plants in reservoirs, lakes, ponds, irrigation ditches, and other potential sources of potable water.
Cupric sulfate is designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance.
Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 10 lb or 45.4 kg. The toll free number of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202) 426-2675. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).
A significant drop in metabolic reserves was noted in cupric sulfate treated snails. Free amino acid levels dropped and the lactate level increased. The effects of copper treatment on rates of metabolite oxidation and ammonia production in the presence of exogenously added alpha-ketoglutarate were evaluated. A 92% drop in alpha-ketoglutarate dehydrogenase, a 33% drop in alanine aminotransferase, and a 78% rise in glucose 6-phosphatase were recorded. Molluscicidal activity of copper was due to a metabolic block in the tricarboxylic acid cycle at the alpha-ketoglutarate level.
ACUTE IV INFUSION OF 300 MG COPPER SULFATE IN CONSCIOUS SHEEP CAUSED AN INCREASE FROM 10.3 TO 22.5 TORR IN MEAN PULMONARY ARTERY PRESSURE & PULMONARY ARTERY WEDGE PRESSURE FROM 3.5 TO 7.6 TORR, WHEREAS SYSTEMIC ARTERIAL PRESSURE INCREASED FROM 95 TO 102 TORR. CARDIAC OUTPUT DECREASED FROM 4.7 TO 3.3 L/MIN. PULMONARY VASCULAR RESISTANCE & SYSTEMIC VASCULAR RESISTANCE INCREASED TO 320 & 160% OF BASE LINE, RESPECTIVELY. THIS PULMONARY HYPERTENSION WAS PRODUCED BY STIMULATION OF THE ALPHA-ADRENERGIC NERVOUS SYSTEM.
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)
Agents counteracting or neutralizing the action of POISONS.
Agents that cause vomiting. They may act directly on the gastrointestinal tract, bringing about emesis through local irritant effects, or indirectly, through their effects on the chemoreceptor trigger zone in the postremal area near the medulla.
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.
Used to detect and remove trace amounts of water from alcohols and other organic compounds; Also used as a pesticide (fungicide, molluscicide, bacteriostat, herbicide, and algaecide), a micronutrient additive for fertilizer and animal feed, a froth flotation agent, a component of electroplating solutions, a component of chromated copper arsenate, an agent for leather tanning and hide preservation, a titration reagent, an antidote for white phosphorus poisoning, formerly an emetic (discontinued due to toxicity), and a veterinary drug (nutritional factor, astringent antiseptic, and fungicidal agent); [HSDB]
Electroplating [Category: Plate]
Preparing and mounting animal skins (taxidermy) [Category: Hobbies]
The medicinal use of copper as an emetic was discontinued because of its toxicity.
For Copper(II) sulfate (USEPA/OPP Pesticide Code: 024408) ACTIVE products with label matches. /SRP: Registered for use in the U.S. but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./
Anhydr salt for detecting and removing trace amounts of water from alcohols and other organic compds; as fungicide
(1985) 1.03X10+9 g
(1986) 1.14X10+9 g
2023: 2,500,000,000 - <4,000,000,000 lb
(1983) 3.72X10+7 g
REACTION OF SCRAP OR SHOT COPPER WITH DILUTE SULFURIC ACID AND AIR; BY-PRODUCT RECOVERED BY CRYSTALLIZATION FROM COPPER REFINERY LIQUORS /SRP: BLUE SALT IS DEHYDRATED BY HEATING TO ANHYDROUS CUPRIC SULFATE./
Action of dilute sulfuric acid on copper or copper oxide (often as oxide ores) in large quantities with evaporation and crystalization.
Copper + sulphuric acid (salt formation); byproduct of copper electrolysis and etching process (product is generally only suitable for agricultural purposes)
Produced from careful dehydration of the pentahydrate at 250 °C; an impure product can also be produced from copper metal and hot sulfuric acid.
USEPA/OPP Pesticide Code 024408; Trade Names: None listed.
Grade: Technical, CP, NF, also sold as monohydrate. Available as crystals or powder.
Crystals; wettable powder; suspension concentrate
Various crystal sizes: medium, large liquid, powder (snow) form, granular, water soluble
For more Formulations/Preparations (Complete) data for COPPER(II) SULFATE (17 total), please visit the HSDB record page.
Plastics -> Polymer Type -> N.a.
Cosmetics -> Skin conditioning
Plastics -> Pigments agents
ALGICIDES
Textiles, apparel, and leather manufacturing
Sulfuric acid copper(2+) salt (1:1): ACTIVE
Sulfuric acid, copper(2+) salt (1:?): INACTIVE
The cmpd, eg cupric sulfate, cupric chloride, cupric acetate and cupric nitrate, showed excellent preservation of mosses and lichens, and very good preservation of ferns and grasses.
... The highest utilized copper cmpd in the USA is copper sulfate.
COPPER(II) CHLORIDE IS A READILY AVAILABLE FORM OF COPPER IN FEEDING TRIALS WHICH COMPARES FAVORABLY WITH COPPER SULFATE IN CATTLE AND SWINE TRIALS.
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)