T3DB: Copper lactate

Identification Taxonomy Biological Properties Physical Properties Toxicity Profile Spectra Concentrations Links References Gene Regulation Targets (6)XML

Targets (6)

Record Information

Version

2.0

Creation Date

2009-06-19 21:58:29 UTC

Update Date

2014-12-24 20:23:26 UTC

Accession Number

T3D1228

Identification

Common Name

Copper lactate

Class

Small Molecule

Description

Copper lactate is a chemical compound of copper. Copper is a chemical element with the symbol Cu and atomic number 29. Copper is an essential elements in plants and animals as it is required for the normal functioning of more than 30 enzymes. It occurs naturally throughout the environment in rocks, soil, water, and air. (6, 7)

Compound Type

Copper Compound
Industrial/Workplace Toxin
Organic Compound
Organometallic
Synthetic Compound

Chemical Structure

MOL SDF PDB SMILES InChI

Synonyms

Synonym
Copper lactic acid
Cupric lactate
Lactic acid, copper(2+) salt (2:1)

Chemical Formula

C₆H₁₀CuO₆

Average Molecular Mass

241.686 g/mol

Monoisotopic Mass

240.977 g/mol

CAS Registry Number

814-81-3

IUPAC Name

(2-hydroxy-3-oxopropoxy)cuprio 2-hydroxypropanoate

Traditional Name

(2-hydroxy-3-oxopropoxy)cuprio 2-hydroxypropanoate

SMILES

CC(O)C(=O)O[Cu]OCC(O)C=O

InChI Identifier

InChI=1S/C3H5O3.C3H6O3.Cu/c4-1-3(6)2-5;1-2(4)3(5)6;/h1,3,6H,2H2;2,4H,1H3,(H,5,6);/q-1;;+2/p-1

InChI Key

InChIKey=SNMSNCQXWYNVQP-UHFFFAOYSA-M

Chemical Taxonomy

Description

belongs to the class of organic compounds known as sugar acids and derivatives. Sugar acids and derivatives are compounds containing a saccharide unit which bears a carboxylic acid group.

Kingdom

Organic compounds

Super Class

Organic oxygen compounds

Class

Organooxygen compounds

Sub Class

Carbohydrates and carbohydrate conjugates

Direct Parent

Sugar acids and derivatives

Alternative Parents

Substituents

Sugar acid
Monosaccharide
Alpha-hydroxyaldehyde
Secondary alcohol
Carboxylic acid salt
Organic metal salt
Organic transition metal salt
Monocarboxylic acid or derivatives
Carboxylic acid derivative
Organic oxide
Hydrocarbon derivative
Organic salt
Carbonyl group
Aldehyde
Alcohol
Aliphatic acyclic compound

Molecular Framework

Aliphatic acyclic compounds

External Descriptors

Not Available

Biological Properties

Status

Detected and Not Quantified

Origin

Exogenous

Cellular Locations

Membrane

Biofluid Locations

Not Available

Tissue Locations

Not Available

Pathways

Not Available

Applications

Not Available

Biological Roles

Not Available

Chemical Roles

Not Available

Physical Properties

State

Solid

Appearance

White powder.

Experimental Properties

Property	Value
Melting Point	Not Available
Boiling Point	Not Available
Solubility	Not Available
LogP	Not Available

Predicted Properties

Property	Value	Source
Water Solubility	276 g/L	ALOGPS
logP	-0.75	ALOGPS
logP	-2.4	ChemAxon
logS	0.06	ALOGPS
pKa (Strongest Acidic)	12.66	ChemAxon
pKa (Strongest Basic)	-3.7	ChemAxon
Physiological Charge	0	ChemAxon
Hydrogen Acceptor Count	5	ChemAxon
Hydrogen Donor Count	2	ChemAxon
Polar Surface Area	93.06 Å²	ChemAxon
Rotatable Bond Count	7	ChemAxon
Refractivity	36.16 m³·mol⁻¹	ChemAxon
Polarizability	17.51 Å³	ChemAxon
Number of Rings	0	ChemAxon
Bioavailability	1	ChemAxon
Rule of Five	Yes	ChemAxon
Ghose Filter	Yes	ChemAxon
Veber's Rule	Yes	ChemAxon
MDDR-like Rule	Yes	ChemAxon

Spectra

Spectrum Type	Description	Splash Key	Deposition Date	View
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 10V, Positive	splash10-006x-5190000000-b8373d1339f1d121866b	2019-02-22	View Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 20V, Positive	splash10-0fk9-5940000000-6c62ff1081cd9f84d5a6	2019-02-22	View Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 40V, Positive	splash10-05fr-9000000000-adec84c528e68cf4cc52	2019-02-22	View Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 10V, Negative	splash10-000i-1590000000-b88474d3deb9a00e9ad0	2019-02-23	View Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 20V, Negative	splash10-007a-9620000000-0043fa04fab51281d5a0	2019-02-23	View Spectrum
Predicted LC-MS/MS	Predicted LC-MS/MS Spectrum - 40V, Negative	splash10-05fr-9300000000-18b6cf84d207e359f98c	2019-02-23	View Spectrum

Toxicity Profile

Route of Exposure

Oral (6) ; inhalation (6) ; dermal (6)

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. (6, 4, 1, 9)

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. (6, 8)

Toxicity Values

Not Available

Lethal Dose

10 to 20 grams for an adult human (copper salts). (3)

Carcinogenicity (IARC Classification)

No indication of carcinogenicity to humans (not listed by IARC).

Uses/Sources

Not Available

Minimum Risk Level

Acute Oral: 0.01 mg/kg/day (5) Intermediate Oral: 0.01 mg/kg/day (5)

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. (7, 8)

Symptoms

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. (7, 8)

Treatment

Not Available

Normal Concentrations

Not Available

Abnormal Concentrations

Not Available

External Links

DrugBank ID

Not Available

HMDB ID

Not Available

PubChem Compound ID

25021466

ChEMBL ID

Not Available

ChemSpider ID

Not Available

KEGG ID

Not Available

UniProt ID

Not Available

OMIM ID

ChEBI ID

Not Available

BioCyc ID

Not Available

CTD ID

Not Available

Stitch ID

Copper lactate

PDB ID

Not Available

ACToR ID

Not Available

Wikipedia Link

Not Available

References

Synthesis Reference

Not Available

MSDS

Not Available

General References

Brewer GJ: A brand new mechanism for copper toxicity. J Hepatol. 2007 Oct;47(4):621-2. Epub 2007 Jul 23. [17697726 ]
Bardsley PA, Howard P, DeBacker W, Vermeire P, Mairesse M, Ledent C, Radermecker M, Bury T, Ansquer J: Two years treatment with almitrine bismesylate in patients with hypoxic chronic obstructive airways disease. Eur Respir J. 1991 Mar;4(3):308-10. [1907566 ]
Baselt RC (2000). Disposition of Toxic Drugs and Chemicals in Man, 5th ed. Foster City, CA: Chemical Toxicology Institute.
Baxter PJ, Adams PH, & Aw TC (2000). Hunter's Diseases of Occupations. 9th ed. New York, NY: Oxford University Press Inc.
ATSDR - Agency for Toxic Substances and Disease Registry (2001). Minimal Risk Levels (MRLs) for Hazardous Substances. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]
Wikipedia. Copper. Last Updated 29 May 2009. [Link]
ATSDR - Agency for Toxic Substances and Disease Registry (2004). Toxicological profile for copper. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]
International Programme on Chemical Safety (IPCS) INCHEM (1998). Environmental Health Criteria for Copper. [Link]
US Environmental Protection Agency (2008). Drinking Water Health Advisory for 2,4-Dinitrotoluene and 2,6-Dinitrotoluene. [Link]

Gene Regulation

Up-Regulated Genes

Not Available

Down-Regulated Genes

Not Available

Targets

Target Details

1. Glucose-6-phosphate 1-dehydrogenase

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

Brewer GJ: A brand new mechanism for copper toxicity. J Hepatol. 2007 Oct;47(4):621-2. Epub 2007 Jul 23. [17697726 ]
Baxter PJ, Adams PH, & Aw TC (2000). Hunter's Diseases of Occupations. 9th ed. New York, NY: Oxford University Press Inc.
Wikipedia. Copper. Last Updated 29 May 2009. [Link]
US Environmental Protection Agency (2008). Drinking Water Health Advisory for 2,4-Dinitrotoluene and 2,6-Dinitrotoluene. [Link]

Target Details

2. Glutathione reductase, mitochondrial

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

Brewer GJ: A brand new mechanism for copper toxicity. J Hepatol. 2007 Oct;47(4):621-2. Epub 2007 Jul 23. [17697726 ]
Baxter PJ, Adams PH, & Aw TC (2000). Hunter's Diseases of Occupations. 9th ed. New York, NY: Oxford University Press Inc.
Wikipedia. Copper. Last Updated 29 May 2009. [Link]
US Environmental Protection Agency (2008). Drinking Water Health Advisory for 2,4-Dinitrotoluene and 2,6-Dinitrotoluene. [Link]

Target Details

3. Serum paraoxonase/arylesterase 1

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

Brewer GJ: A brand new mechanism for copper toxicity. J Hepatol. 2007 Oct;47(4):621-2. Epub 2007 Jul 23. [17697726 ]
Baxter PJ, Adams PH, & Aw TC (2000). Hunter's Diseases of Occupations. 9th ed. New York, NY: Oxford University Press Inc.
Wikipedia. Copper. Last Updated 29 May 2009. [Link]
US Environmental Protection Agency (2008). Drinking Water Health Advisory for 2,4-Dinitrotoluene and 2,6-Dinitrotoluene. [Link]

Target Details

4. Serum paraoxonase/lactonase 3

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

Brewer GJ: A brand new mechanism for copper toxicity. J Hepatol. 2007 Oct;47(4):621-2. Epub 2007 Jul 23. [17697726 ]
Baxter PJ, Adams PH, & Aw TC (2000). Hunter's Diseases of Occupations. 9th ed. New York, NY: Oxford University Press Inc.
Wikipedia. Copper. Last Updated 29 May 2009. [Link]
US Environmental Protection Agency (2008). Drinking Water Health Advisory for 2,4-Dinitrotoluene and 2,6-Dinitrotoluene. [Link]

Target Details

5. Alpha-synuclein

General Function:: Not Available
Specific Function:: Not Available
Gene Name:: SNCA
Uniprot ID:: P37840
Molecular Weight:: 14460.155 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 ]

Target Details

6. Amyloid beta A4 protein

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 ]

Copper lactate (T3D1228)

Structure for T3D1228: Copper lactate

Targets

References

References

References

References

References

References