Copper(II) Sulphate
Copper(II) Sulphate Uses, Dosage, Side Effects, Food Interaction and all others data.
Copper(II) Sulphate is a salt created by treating cupric oxide with sulfuric acid. This forms as large, bright blue crystals containing five molecules of water (CuSO4∙5H2O) and is also known as blue vitriol. The anhydrous salt is created by heating the hydrate to 150 °C (300 °F). Copper(II) Sulphate is used primarily for agricultural purposes, as a pesticide, germicide, feed additive, and soil additive. Some of its secondary uses are as a raw material in the preparation of other copper compounds, as a reagent in analytic chemistry, as an electrolyte for batteries and electroplating baths, and in medical practice as a locally applied fungicide, bactericide, and astringent .
Copper is an essential trace element and an important catalyst for heme synthesis and iron absorption. After zinc and iron, copper is the third most abundant trace element found in the human body. Copper is a noble metal and its properties include high thermal and electrical conductivity, low corrosion, alloying ability, and malleability. Copper is a component of intrauterine contraceptive devices (IUD) and the release of copper is necessary for their important contraceptive effects. The average daily intake of copper in the USA is approximately 1 mg Cu with the diet being a primary source .
Interestingly, the dysregulation of copper has been studied with a focus on neurodegenerative diseases, such as Wilson’s disease, Alzheimer’s disease, and Parkinson’s disease. Data from clinical observations of the neurotoxic effects of copper may provide the basis for future treatments affecting copper and its homeostasis .
| Trade Name | Copper(II) Sulphate |
| Generic | Cupric sulfate |
| Cupric sulfate Other Names | Copper monosulfate, Copper monosulphate, Copper sulfate, Copper sulfate (1:1), Copper sulphate, Copper(2+) sulfate, Copper(II) sulphate |
| Type | |
| Formula | CuO4S |
| Weight | Average: 159.609 Monoisotopic: 158.881330257 |
| 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 . |
| Groups | Approved |
| Therapeutic Class | |
| Manufacturer | |
| Available Country | |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Copper(II) Sulphate is a compound used as an intravenous copper supplement for Total Parenteral Nutrition (TPN).
Elemental use in copper deficiency
Copper and copper containing compounds are broadly used in medical practice. Metallic copper is used already for many years in dental fillings and in copper intrauterine devices (IUD) for reversible contraception. Ointments containing copper, which release copper ions that are absorbed by the skin in the management of cramps, disturbances of renal function, peripheral, venous hypostatic circulatory disturbances, rheumatic disease and swelling associated with trauma. There are also cosmetic facial creams containing copper as their main active ingredient .
Copper(II) Sulphate is also used to associated treatment for these conditions: Copper Deficiency, Skin disinfection
How Copper(II) Sulphate works
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 .
Copper(II) Sulphate 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 .
Toxicity
Acute oral toxicity (LD50): 300 mg/kg in rats .
Copper sulfate ingestion (accidental or deliberate) is a rare form of poisoning usually limited to the Indian subcontinent. Though the rates are on the decline, it is essential that physicians are aware of its lethal complications and management strategies. The main complications of copper sulfate ingestion include intravascular hemolysis, methemoglobinaemia, acute kidney injury, and rhabdomyolysis .
Severe gastrointestinal effects may occur with acute overdosage. In extreme or long-term overdosage, symptoms may be similar to those of Wilson's disease, a disease in which the liver does not filter copper adequately and copper accumulates in the liver, brain, eyes, and other organs. Gradually, high copper levels may cause life-threatening organ damage .
Ingestion of more than 15 mg of copper has been reported to be toxic to humans. In a survey of human clinical case studies, 5.3 mg/day was the lowest oral dose at which local gastrointestinal irritation was seen. Ingestion of gram quantities of copper sulfate resulted in death by suicide, whereas less severe effects were reported from estimated copper doses of 40 to 50 mg from ingestion of carbonated beverages in contact with copper containers. Limited data are available on the chronic toxicity of copper. The hazard from dietary intakes of up to 5 mg/day appears to be low .
Treatment of cupric sulfate toxicity is symptomatic and may involve the use of a chelating agent (e.g. penicillamine, trientine and zinc) to remove any excessive metal that has been absorbed. In addition, dialysis may be useful .
Food Interaction
No interactions found.Volume of Distribution
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 .
Elimination Route
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 .
Half Life
The biological half-life of copper from the diet is 13-33 days with biliary excretion being the primary route of elimination .
Elimination Route
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 .
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