 sulfate Chemical Structure.png)
Physicochemical Properties
| Molecular Formula | CUO4S |
| Molecular Weight | 159.61 |
| Exact Mass | 248.934 |
| CAS # | 7758-98-7 |
| PubChem CID | 24462 |
| Appearance |
Grayish-white to greenish-white rhombic crystals or amorphous powder /SRP: somewhat wet/ White when dehydrated Gray to white and has rhombic crystals |
| Density | 3.603 g/mL at 25 °C(lit.) |
| Boiling Point | 330ºC at 760 mmHg |
| Melting Point | 200 °C (dec.)(lit.) |
| Vapour Pressure | 3.35E-05mmHg at 25°C |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 4 |
| Rotatable Bond Count | 0 |
| Heavy Atom Count | 6 |
| Complexity | 62.2 |
| Defined Atom Stereocenter Count | 0 |
| SMILES | O=S([O-])(=O)[O-].[Cu+2] |
| InChi Key | ARUVKPQLZAKDPS-UHFFFAOYSA-L |
| InChi Code | InChI=1S/Cu.H2O4S/c;1-5(2,3)4/h;(H2,1,2,3,4)/q+2;/p-2 |
| Chemical Name | copper;sulfate |
| Synonyms | Cupric sulfate |
| HS Tariff Code | 2934.99.9001 |
| Storage |
Powder-20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| Shipping Condition | Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs) |
Biological Activity
| ADME/Pharmacokinetics |
Absorption, Distribution and Excretion 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. Metabolism / Metabolites 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) Biological Half-Life The biological half-life of copper from the diet is 13-33 days with biliary excretion being the primary route of elimination. |
| Toxicity/Toxicokinetics |
Toxicity Summary 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) Protein Binding 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. Toxicity Data LD50: 300 mg/kg (Oral, Rat) (L341) LD50: 20 mg/kg (Intraperitoneal, Rabbit) (L341) LD50: 43 mg/kg (Subcutaneous, Rat) (L341) LD50: 49 mg/kg (Intravenous, Rat) (L341) Interactions 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. Non-Human Toxicity Values LD50 Rat oral 300 mg/kg body weight LD50 Rabbit Oral 125 mg/kg body weight LD100 Mouse Oral 50 mg/kg body weight /from table/ |
| References |
[1]. Biochemical reagents[M]//Methods of Enzymatic Analysis. Academic Press, 1965: 967-1037. |
| Additional Infomation |
Therapeutic Uses Antidotes; Emetics; Fungicides, Industrial /SRP: EXTERNAL/ ANTIDOTE FOR WHITE PHOSPHORUS POISONING. /SRP: FORMER USE/ A 0.1% soln of copper sulfate has been used for gastric lavage in phosphorus poisoning; it must be removed promptly to avoid copper poisoning. Topical application of a 1% soln is of value for phosphorus burns of the skin. EXPT USE: IN EXPT WITH RATS TO FIND SIMPLE EFFICIENT ANTIDOTE FOR PHOSPHORUS BURNS, USE OF 5% COPPER SULFATE WAS HIGHLY TOXIC. SOLN OF 5% SODIUM BICARBONATE WITH 1% HYDROXYETHYL-CELLULOSE, 3% COPPER SULFATE & LAURYL SULFATE NEUTRALIZES PROCESS OF BURNING PHOSPHORUS. For more Therapeutic Uses (Complete) data for COPPER(II) SULFATE (11 total), please visit the HSDB record page. Drug Warnings ... Its routine use as an emetic is not recommended, because of the potential toxicity of improperly prepared soln and the hazards attending the use of large, corrosive doses. Overdose may be poisonous (enteritis, hepatitis, nephritis). MAY CAUSE DRAMATIC INCR IN MORTALITY OF TURKEYS GIVEN BLACKHEAD CONTROL DRUGS CONTAINING ARSENIC & EXPOSED TO BLACKHEAD. CUPRIC ... SULFATE /AS EMETIC/ OFTEN IS EFFECTIVE, BUT POTENTIAL HEMOLYTIC & RENAL TOXICITY IS TOO GREAT TO RECOMMEND USE. Pharmacodynamics 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. |
Solubility Data
| Solubility (In Vitro) | H2O : 100 mg/mL (626.53 mM; with sonication) |
| Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples. Injection Formulations (e.g. IP/IV/IM/SC) Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] *Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline) Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline) Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline) Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil) Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Oral Formulations Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). Oral Formulation 3: Dissolved in PEG400 Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose Oral Formulation 6: Mixing with food powders Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 6.2653 mL | 31.3264 mL | 62.6527 mL | |
| 5 mM | 1.2531 mL | 6.2653 mL | 12.5305 mL | |
| 10 mM | 0.6265 mL | 3.1326 mL | 6.2653 mL |