Explore a selection of our essential drug information below, or:
Identification
- Generic Name
- Chromium gluconate
- DrugBank Accession Number
- DB14528
- Background
Not Available
- Type
- Small Molecule
- Groups
- Approved
- Structure
Structure for Chromium gluconate (DB14528)
- Weight
- Average: 637.437
Monoisotopic: 637.091939 - Chemical Formula
- C18H33CrO21
- Synonyms
- Not Available
Pharmacology
- Indication
Indicated for use as a supplement to intravenous solutions given for total parenteral nutrition (TPN), to maintain chromium serum levels and to prevent depletion of endogenous stores and subsequent deficiency symptoms Label.
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Trivalent chromium is part of glucose tolerance factor, an essential activator of insulin-mediated reactions. Chromium helps to maintain normal glucose metabolism and peripheral nerve function. Chromium increases insulin binding to cells, increases insulin receptor density and activates insulin receptor kinase leading to enhanced insulin sensitivity 2. In chromium deficiency, intravenous administration of chromium resulted in normalization of the glucose tolerance curve from the diabetic-like curve typical of chromium deficiency Label.
- Mechanism of action
Chromium is an essential nutrient involved in the metabolism of glucose, insulin and blood lipids. Its role in potentiating insulin signalling cascades has been implicated in several studies. Chromium upregulates insulin-stimulated insulin signal transduction via affecting effector molecules downstream of the insulin receptor (IR). IR-mediated signalling pathway involves phoshorylation of multiple intracellular domains and protein kinases, and downstream effector molecules 3. Upon activation by ligands, intracellular β-subunit of IR autophosphorylates and activates tyrosine kinase domain of the IR, followed by activation and phosphorylation of regulatory proteins and downstream signalling effectors including phosphatidylinositol 2-kinase (PI3K). PI3K activates further downstream reaction cascades to activate protein kinase B (Akt) to ultimately promote translocation of glucose transporter-4 (Glut4)-vesicles from the cytoplasm to the cell surface and regulate glucose uptake 3. Chromium enhances the kinase activity of insulin receptor β and increases the activity of downstream effectors, pI3-kinase and Akt.
Under insulin-resistant conditions, chromium also promotes GLUT-4 transporter translocation that is independent of activity of IR, IRS-1, PI3-kinase, or Akt; chromium mediates cholesterol efflux from the membranes via increasing fluidity of the membrane by decreasing the membrane cholesterol and upregulation of sterol regulatory element-binding protein 3. As a result, intracellular GLUT-4 transporters are stimulated to translocate from intracellular to the plasma membrane, leading to enhanced glucose uptake in muscle cells 8. Chromium attenuates the activity of PTP-1B in vitro, which is a negative regulator of insulin signaling. It also alleviates ER stress that is observed to be elevated the suppression of insulin signaling. ER stress is thought to activate c-Jun N-terminal kinase (JNK), which subsequently induces serine phosphorylation of IRS and aberration of insulin signalling 3. Transient upregulation of AMPK by chromium also leads to increased glucose uptake 3.
Target Actions Organism UCytochrome b5 Not Available Humans - Absorption
Chromium compounds are both absorbed by the lung and the gastrointestinal tract. Oral absorption of chromium compounds in humans can range between 0.5% and 10%, with the hexavalent (VI) chromium more easily absorbed than the trivalent (III) form 5. Absorption of chromium from the intestinal tract is low, ranging from less than 0.4% to 2.5% of the amount consumed 7. Vitamin C and the vitamin B niacin is reported to enhance chromium absorption 7.
Most hexavalent Cr (VI) undergoes partial intragastric reduction to Cr (III) upon absorption, which is an action mainly mediated by sulfhydryl groups of amino acids 5. Cr (VI) readily penetrates cell membranes and chromium can be found in both erythrocytes and plasma after gastrointestinal absorption of Cr (IV). In comparison, the presence of chromium is limited to the plasma as Cr (III) displays poor cell membrane penetration 5. Once transported through the cell membrane, Cr (VI) is rapidly reduced to Cr (III), which subsequently binds to macromolecules or conjugate with proteins. Cr (III) may be bound to transferrin or other plasma proteins, or as complexes, such as glucose tolerance factor (GTF).
- Volume of distribution
Absorbed chromium is distributed to all tissues of the body and its distribution in the body depends on the species, age, and chemical form 8. Circulating Cr (III) following oral or parenteral administration of different compounds can be taken up by tissues and accumulates in the liver, kidney, spleen, soft tissue, and bone 7.
- Protein binding
In the blood, 95% of chromium (III) is bound to large molecular mass proteins, such as transferrin, while a small proportion associates with low molecular mass oligopeptides 6. Serum chromium is bound to transferrin in the beta globulin fraction Label.
- Metabolism
The metabolism of Cr (VI) involves reduction by small molecules and enzyme systems to generate Cr (III) and reactive intermediates. During this process, free radicals can be generated, which is thought to induce damage of cellular components and cause toxicity of chromium 6. The metabolites bind to cellular constituents 5.
- Route of elimination
Absorbed chromium is excreted mainly in the urine, accounting for 80% of total excretion of chromium; small amounts are lost in hair, perspiration and bile 5. Chromium is excreted primarily in the urine by glomerular filtration or bound to a low molecular-weight organic transporter 8.
- Half-life
The elimination half-life of hexavalent chromium is 15 to 41 hours 5.
- Clearance
Excretion of chromium is via the kidneys ranges from 3 to 50 μg/day Label. The 24-hour urinary excretion rates for normal human subjects are reported to be 0.22 μg/day 8.
- Adverse Effects
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Oral LD50 for Cr (VI) is 135 - 175 mg/kg in mouse and 46 - 113 mg/kg in rat 5. Oral LD50 for Cr (III) in rat is >2000 mg/kg 5. LD50 of chromium (III) oxide in rats is reported to be > 5g/kg 6. Other LD50 values reported for rats include: 3.5 g/kg (CI 3.19-3.79 g/kg) for chromium sulphate; 11.3 g/kg for chromium (III) acetate; 3.3 g/kg for chromium nitrate; and 1.5 g/kg for chromium nitrate nonahydrate 6.
Acute overdose of chromium is rare and seriously detrimental effects of hexavalent chromium are primarily the result of chronic low-level exposure 5. In case of overdose with minimal toxicity following acute ingestion, treatment should be symptomatic and supportive 5. There is no known antidote for chromium toxicity.
Hexavalent chromium is a Class A carcinogen by the inhalation route of exposure and Class D by the oral route 5. The oral lethal dose in humans has been estimated to be 1-3 g of Cr (VI); oral toxicity most likely involves gastrointestinal bleeding rather than systemic toxicity 5. Chronic exposure may cause damage to the following organs: kidneys, lungs, liver, upper respiratory tract MSDS. Soluble chromium VI compounds are human carcinogens. Hexavalent chromium compounds were mutagenic in bacteria assays and caused chromosome aberrations in mammalian cells. There have been associations of increased frequencies of chromosome aberrations in lymphocytes from chromate production workers 4. In human cells in vitro, Cr (VI) caused chromosomal aberrations, sister chromatid exchanges and oxidative DNA damage 5.
- Pathways
- Not Available
- Pharmacogenomic Effects/ADRs
- Not Available
Interactions
- Drug Interactions
- This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.
Drug Interaction Integrate drug-drug
interactions in your softwareAbacavir Abacavir may decrease the excretion rate of Chromium gluconate which could result in a higher serum level. Aceclofenac Aceclofenac may decrease the excretion rate of Chromium gluconate which could result in a higher serum level. Acemetacin Acemetacin may decrease the excretion rate of Chromium gluconate which could result in a higher serum level. Acetaminophen Acetaminophen may decrease the excretion rate of Chromium gluconate which could result in a higher serum level. Acetazolamide Acetazolamide may increase the excretion rate of Chromium gluconate which could result in a lower serum level and potentially a reduction in efficacy. - Food Interactions
- Not Available
Categories
- Drug Categories
- Chemical TaxonomyProvided by Classyfire
- Description
- This compound belongs to the class of organic compounds known as sugar acids and derivatives. These 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
- Medium-chain hydroxy acids and derivatives / Medium-chain fatty acids / Beta hydroxy acids and derivatives / Hydroxy fatty acids / Monosaccharides / Secondary alcohols / Carboxylic acid salts / Polyols / Carboxylic acids / Monocarboxylic acids and derivatives show 6 more
- Substituents
- Alcohol / Aliphatic acyclic compound / Beta-hydroxy acid / Carbonyl group / Carboxylic acid / Carboxylic acid derivative / Carboxylic acid salt / Fatty acid / Fatty acyl / Gluconic_acid show 15 more
- Molecular Framework
- Not Available
- External Descriptors
- Not Available
- Affected organisms
- Not Available
Chemical Identifiers
- UNII
- V236ZVR3RL
- CAS number
- 33661-40-4
- InChI Key
- ANPGUZATXCGJJH-OPDGVEILSA-K
- InChI
- InChI=1S/3C6H12O7.Cr/c3*7-1-2(8)3(9)4(10)5(11)6(12)13;/h3*2-5,7-11H,1H2,(H,12,13);/q;;;+3/p-3/t3*2-,3-,4+,5-;/m111./s1
- IUPAC Name
- chromium(3+) tris((2R,3S,4R,5R)-2,3,4,5,6-pentahydroxyhexanoate)
- SMILES
- [Cr+3].OC[C@@H](O)[C@@H](O)[C@H](O)[C@@H](O)C([O-])=O.OC[C@@H](O)[C@@H](O)[C@H](O)[C@@H](O)C([O-])=O.OC[C@@H](O)[C@@H](O)[C@H](O)[C@@H](O)C([O-])=O
References
- General References
- Wallach S: Clinical and biochemical aspects of chromium deficiency. J Am Coll Nutr. 1985;4(1):107-20. [Article]
- Anderson RA: Chromium in the prevention and control of diabetes. Diabetes Metab. 2000 Feb;26(1):22-7. [Article]
- Hua Y, Clark S, Ren J, Sreejayan N: Molecular mechanisms of chromium in alleviating insulin resistance. J Nutr Biochem. 2012 Apr;23(4):313-9. doi: 10.1016/j.jnutbio.2011.11.001. [Article]
- CHROMIUM, ELEMENTAL - National Library of Medicine HSDB ... - Toxnet - NIH [Link]
- CHROMIUM COMPOUNDS - National Library of Medicine HSDB ... - Toxnet - NIH [Link]
- Chromium Toxicological Overview - Health Protection Agency - Gov.uk [Link]
- Dietary Supplement Fact Sheet: Chromium [Link]
- Dailymed Label: DIVISTA - chromium picolinate capsule [Link]
- External Links
- ChemSpider
- 32701256
Clinical Trials
- Clinical Trials
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Pharmacoeconomics
- Manufacturers
- Not Available
- Packagers
- Not Available
- Dosage Forms
- Not Available
- Prices
- Not Available
- Patents
- Not Available
Properties
- State
- Not Available
- Experimental Properties
- Not Available
- Predicted Properties
Property Value Source Water Solubility 22.8 mg/mL ALOGPS logP -2 ALOGPS logP -3.4 Chemaxon logS -1.4 ALOGPS pKa (Strongest Acidic) 3.39 Chemaxon pKa (Strongest Basic) -3 Chemaxon Physiological Charge -1 Chemaxon Hydrogen Acceptor Count 7 Chemaxon Hydrogen Donor Count 5 Chemaxon Polar Surface Area 141.28 Å2 Chemaxon Rotatable Bond Count 15 Chemaxon Refractivity 49.11 m3·mol-1 Chemaxon Polarizability 16.62 Å3 Chemaxon Number of Rings 0 Chemaxon Bioavailability 0 Chemaxon Rule of Five No Chemaxon Ghose Filter No Chemaxon Veber's Rule No Chemaxon MDDR-like Rule No Chemaxon - Predicted ADMET Features
- Not Available
Spectra
- Mass Spec (NIST)
- Not Available
- Spectra
- Not Available
- Chromatographic Properties
Collision Cross Sections (CCS)
Adduct CCS Value (Å2) Source type Source [M-H]- 144.1697502 predictedDarkChem Lite v0.1.0 [M+H]+ 146.5715502 predictedDarkChem Lite v0.1.0 [M+Na]+ 144.3052502 predictedDarkChem Lite v0.1.0
Targets
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- General Function
- Cytochrome b5 is a membrane-bound hemoprotein functioning as an electron carrier for several membrane-bound oxygenases
- Specific Function
- cytochrome-c oxidase activity
- Gene Name
- CYB5A
- Uniprot ID
- P00167
- Uniprot Name
- Cytochrome b5
- Molecular Weight
- 15329.985 Da
References
- Jannetto PJ, Antholine WE, Myers CR: Cytochrome b(5) plays a key role in human microsomal chromium(VI) reduction. Toxicology. 2001 Feb 28;159(3):119-33. [Article]
Carriers
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- General Function
- Transferrins are iron binding transport proteins which can bind two Fe(3+) ions in association with the binding of an anion, usually bicarbonate. It is responsible for the transport of iron from sites of absorption and heme degradation to those of storage and utilization. Serum transferrin may also have a further role in stimulating cell proliferation
- Specific Function
- enzyme binding
- Gene Name
- TF
- Uniprot ID
- P02787
- Uniprot Name
- Serotransferrin
- Molecular Weight
- 77049.175 Da
References
- Moshtaghie AA, Ani M, Bazrafshan MR: Comparative binding study of aluminum and chromium to human transferrin. Effect of iron. Biol Trace Elem Res. 1992 Jan-Mar;32:39-46. [Article]
Drug created at July 12, 2018 19:28 / Updated at January 08, 2021 01:07