CUPROUS IODIDE
General Information
| Mainterm | CUPROUS IODIDE |
| Doc Type | NIL |
| CAS Reg.No.(or other ID) | 7681-65-4 |
| Regnum |
178.2010 177.2470 582.80 100.155 184.1265 |
From www.fda.gov
Computed Descriptors
Download SDF| 2D Structure | |
| CID | 6432705 |
| IUPAC Name | copper(1+);iodide |
| InChI | InChI=1S/Cu.HI/h;1H/q+1;/p-1 |
| InChI Key | LSXDOTMGLUJQCM-UHFFFAOYSA-M |
| Canonical SMILES | [Cu+].[I-] |
| Molecular Formula | CuI |
| Wikipedia | cuprous iodide |
From Pubchem
Computed Properties
| Property Name | Property Value |
|---|---|
| Molecular Weight | 190.45 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 1 |
| Rotatable Bond Count | 0 |
| Complexity | 0.0 |
| CACTVS Substructure Key Fingerprint | A A A D c Q A A A A A A A g A E A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A = = |
| Topological Polar Surface Area | 0.0 |
| Monoisotopic Mass | 189.834 |
| Exact Mass | 189.834 |
| Compound Is Canonicalized | True |
| Formal Charge | 0 |
| Heavy Atom Count | 2 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Isotope Atom Count | 0 |
| Covalently-Bonded Unit Count | 2 |
From Pubchem
Toxicity Profile
| Route of Exposure | Oral ; inhalation ; dermal |
|---|---|
| Mechanism of Toxicity | 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. |
| Metabolism | 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. |
| Toxicity Values | None |
| Lethal Dose | 10 to 20 grams for an adult human (copper salts). |
| Carcinogenicity (IARC Classification) | No indication of carcinogenicity to humans (not listed by IARC). |
| Minimum Risk Level | Acute Oral: 0.01 mg/kg/day Intermediate Oral: 0.01 mg/kg/day |
| Health Effects | 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) |
| Treatment | 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. |
| Reference |
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From T3DB
Taxonomic Classification
| Kingdom | Inorganic compounds |
|---|---|
| Superclass | Mixed metal/non-metal compounds |
| Class | Transition metal salts |
| Subclass | Transition metal iodides |
| Intermediate Tree Nodes | Not available |
| Direct Parent | Transition metal iodides |
| Alternative Parents | |
| Molecular Framework | Not available |
| Substituents | Transition metal iodide - Inorganic salt |
| Description | This compound belongs to the class of inorganic compounds known as transition metal iodides. These are inorganic compounds in which the largest halogen atom is Iodine, and the heaviest metal atom is a transition metal. |
From ClassyFire
Targets
- General Function:
- Protein homodimerization activity
- Specific Function:
- Catalyzes the rate-limiting step of the oxidative pentose-phosphate pathway, which represents a route for the dissimilation of carbohydrates besides glycolysis. The main function of this enzyme is to provide reducing power (NADPH) and pentose phosphates for fatty acid and nucleic acid synthesis.
- Gene Name:
- G6PD
- Uniprot ID:
- P11413
- Molecular Weight:
- 59256.31 Da
References
- US Environmental Protection Agency (2008). Drinking Water Health Advisory for 2,4-Dinitrotoluene and 2,6-Dinitrotoluene.: http://www.epa.gov/OGWDW/ccl/pdfs/reg_determine2/healthadvisory_ccl2-reg2_dinitrotoluenes.pdf [17697726 ]
- General Function:
- Nadp binding
- Specific Function:
- Maintains high levels of reduced glutathione in the cytosol.
- Gene Name:
- GSR
- Uniprot ID:
- P00390
- Molecular Weight:
- 56256.565 Da
References
- US Environmental Protection Agency (2008). Drinking Water Health Advisory for 2,4-Dinitrotoluene and 2,6-Dinitrotoluene.: http://www.epa.gov/OGWDW/ccl/pdfs/reg_determine2/healthadvisory_ccl2-reg2_dinitrotoluenes.pdf [17697726 ]
- General Function:
- Protein homodimerization activity
- Specific Function:
- Hydrolyzes the toxic metabolites of a variety of organophosphorus insecticides. Capable of hydrolyzing a broad spectrum of organophosphate substrates and lactones, and a number of aromatic carboxylic acid esters. Mediates an enzymatic protection of low density lipoproteins against oxidative modification and the consequent series of events leading to atheroma formation.
- Gene Name:
- PON1
- Uniprot ID:
- P27169
- Molecular Weight:
- 39730.99 Da
References
- US Environmental Protection Agency (2008). Drinking Water Health Advisory for 2,4-Dinitrotoluene and 2,6-Dinitrotoluene.: http://www.epa.gov/OGWDW/ccl/pdfs/reg_determine2/healthadvisory_ccl2-reg2_dinitrotoluenes.pdf [17697726 ]
- General Function:
- Protein homodimerization activity
- Specific Function:
- Has low activity towards the organophosphate paraxon and aromatic carboxylic acid esters. Rapidly hydrolyzes lactones such as statin prodrugs (e.g. lovastatin). Hydrolyzes aromatic lactones and 5- or 6-member ring lactones with aliphatic substituents but not simple lactones or those with polar substituents.
- Gene Name:
- PON3
- Uniprot ID:
- Q15166
- Molecular Weight:
- 39607.185 Da
References
- US Environmental Protection Agency (2008). Drinking Water Health Advisory for 2,4-Dinitrotoluene and 2,6-Dinitrotoluene.: http://www.epa.gov/OGWDW/ccl/pdfs/reg_determine2/healthadvisory_ccl2-reg2_dinitrotoluenes.pdf [17697726 ]
- General Function:
- Transition metal ion binding
- Specific Function:
- Functions as a cell surface receptor and performs physiological functions on the surface of neurons relevant to neurite growth, neuronal adhesion and axonogenesis. Involved in cell mobility and transcription regulation through protein-protein interactions. Can promote transcription activation through binding to APBB1-KAT5 and inhibits Notch signaling through interaction with Numb. Couples to apoptosis-inducing pathways such as those mediated by G(O) and JIP. Inhibits G(o) alpha ATPase activity (By similarity). Acts as a kinesin I membrane receptor, mediating the axonal transport of beta-secretase and presenilin 1. Involved in copper homeostasis/oxidative stress through copper ion reduction. In vitro, copper-metallated APP induces neuronal death directly or is potentiated through Cu(2+)-mediated low-density lipoprotein oxidation. Can regulate neurite outgrowth through binding to components of the extracellular matrix such as heparin and collagen I and IV. The splice isoforms that contain the BPTI domain possess protease inhibitor activity. Induces a AGER-dependent pathway that involves activation of p38 MAPK, resulting in internalization of amyloid-beta peptide and leading to mitochondrial dysfunction in cultured cortical neurons. Provides Cu(2+) ions for GPC1 which are required for release of nitric oxide (NO) and subsequent degradation of the heparan sulfate chains on GPC1.Beta-amyloid peptides are lipophilic metal chelators with metal-reducing activity. Bind transient metals such as copper, zinc and iron. In vitro, can reduce Cu(2+) and Fe(3+) to Cu(+) and Fe(2+), respectively. Beta-amyloid 42 is a more effective reductant than beta-amyloid 40. Beta-amyloid peptides bind to lipoproteins and apolipoproteins E and J in the CSF and to HDL particles in plasma, inhibiting metal-catalyzed oxidation of lipoproteins. Beta-APP42 may activate mononuclear phagocytes in the brain and elicit inflammatory responses. Promotes both tau aggregation and TPK II-mediated phosphorylation. Interaction with overexpressed HADH2 leads to oxidative stress and neurotoxicity. Also binds GPC1 in lipid rafts.Appicans elicit adhesion of neural cells to the extracellular matrix and may regulate neurite outgrowth in the brain.The gamma-CTF peptides as well as the caspase-cleaved peptides, including C31, are potent enhancers of neuronal apoptosis.N-APP binds TNFRSF21 triggering caspase activation and degeneration of both neuronal cell bodies (via caspase-3) and axons (via caspase-6).
- Gene Name:
- APP
- Uniprot ID:
- P05067
- Molecular Weight:
- 86942.715 Da
References
- Davies P, Fontaine SN, Moualla D, Wang X, Wright JA, Brown DR: Amyloidogenic metal-binding proteins: new investigative pathways. Biochem Soc Trans. 2008 Dec;36(Pt 6):1299-303. doi: 10.1042/BST0361299. [19021544 ]
From T3DB