Peringatan Keamanan

Acute oral toxicity (LD50): 300 mg/kg in rats MSDS.

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 L1827.

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 L1823.

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 L1838.

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 L1821, L1823.

Cupric sulfate

DB06778

small molecule approved

Deskripsi

Cupric sulfate 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). Cupric sulfate 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 L1820.

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 A32221.

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 L1830.

Struktur Molekul 2D

Berat 159.609
Wujud solid

Peta Jejaring Molekuler
Legenda: ObatTargetGenEnzim(Panah → menunjukkan arah efek / relasi)TransporterCarrier

Profil Farmakokinetik

Waktu Paruh (Half-Life) The biological half-life of copper from the diet is 13-33 days with biliary excretion being the primary route of elimination [A32221].
Volume Distribusi 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 [L1828]. 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 [L1838]. 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 [L1838].
Klirens (Clearance) -

Absorpsi

Primarily absorbed in the small intestine L1823. 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) L1838. Copper absorbed from the gastrointestinal tract is transported rapidly to blood serum and deposited in the liver bound to metallothionein L1838. From 20 to 60% of the dietary copper is absorbed L1819.

Metabolisme

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 L1838. 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 L1838.

Rute Eliminasi

This drug is 80% eliminated via the liver in bile. Minimal excretion by the kidney L1823. 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 L1838.

Interaksi Obat

0 Data
Tidak ada data.

Referensi & Sumber

Artikel (PubMed)
  • PMID: 12893385
    Faure A, Mathon L, Poupelin JC, Allaouchiche B, Chassard D: Acute cupric sulfate intoxication: pathophysiology and therapy about a case report. Ann Fr Anesth Reanim. 2003 Jun;22(6):557-9.
  • PMID: 15080347
    Armstrong TA, Cook DR, Ward MM, Williams CM, Spears JW: Effect of dietary copper source (cupric citrate and cupric sulfate) and concentration on growth performance and fecal copper excretion in weanling pigs. J Anim Sci. 2004 Apr;82(4):1234-40. doi: 10.2527/2004.8241234x.
  • PMID: 8253299
    Hebert CD, Elwell MR, Travlos GS, Fitz CJ, Bucher JR: Subchronic toxicity of cupric sulfate administered in drinking water and feed to rats and mice. Fundam Appl Toxicol. 1993 Nov;21(4):461-75.
  • PMID: 15935409
    Lim J, Lawless HT: Oral sensations from iron and copper sulfate. Physiol Behav. 2005 Jun 30;85(3):308-13. doi: 10.1016/j.physbeh.2005.04.018.
  • PMID: 10382557
    Barceloux DG: Copper. J Toxicol Clin Toxicol. 1999;37(2):217-30.

Contoh Produk & Brand

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Menampilkan 8 dari 123 produk.
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