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Record Information
Version2.0
Creation Date2009-03-21 00:46:35 UTC
Update Date2014-12-24 20:22:28 UTC
Accession NumberT3D0640
Identification
Common NameBeryllium bromide
ClassSmall Molecule
DescriptionBeryllium bromide is a bromide of beryllium. Beryllium is a lightweight alkaline earth metal with the atomic number 4. It is a relatively rare element found naturally only combined with other elements in minerals. Bromine is a halogen element with the symbol Br and atomic number 35. Diatomic bromine does not occur naturally, but bromine salts can be found in crustal rock. (11, 7)
Compound Type
  • Beryllium Compound
  • Bromide Compound
  • Industrial/Workplace Toxin
  • Inorganic Compound
  • Pollutant
  • Synthetic Compound
Chemical Structure
Thumb
Synonyms
Synonym
BeBr2
Beryllium dibromide
Chemical FormulaBeBr2
Average Molecular Mass168.820 g/mol
Monoisotopic Mass166.849 g/mol
CAS Registry Number7787-46-4
IUPAC Namedibromoberyllium
Traditional Namedibromoberyllium
SMILESBr[Be]Br
InChI IdentifierInChI=1S/Be.2BrH/h;2*1H/q+2;;/p-2
InChI KeyInChIKey=PBKYCFJFZMEFRS-UHFFFAOYSA-L
Chemical Taxonomy
Description belongs to the class of inorganic compounds known as alkaline earth metal bromides. These are inorganic compounds in which the largest halogen atom is Bromine, and the heaviest metal atom a lanthanide.
KingdomInorganic compounds
Super ClassMixed metal/non-metal compounds
ClassAlkaline earth metal salts
Sub ClassAlkaline earth metal bromides
Direct ParentAlkaline earth metal bromides
Alternative Parents
Substituents
  • Alkaline earth metal bromide
  • Inorganic beryllium salt
  • Inorganic salt
Molecular FrameworkNot Available
External DescriptorsNot Available
Biological Properties
StatusDetected and Not Quantified
OriginExogenous
Cellular Locations
  • Cytoplasm
  • Extracellular
Biofluid LocationsNot Available
Tissue LocationsNot Available
PathwaysNot Available
ApplicationsNot Available
Biological RolesNot Available
Chemical RolesNot Available
Physical Properties
StateSolid
AppearanceWhite crystals.
Experimental Properties
PropertyValue
Melting Point508°C (473°C sublimes )
Boiling PointNot Available
SolubilityNot Available
LogPNot Available
Predicted Properties
PropertyValueSource
logP1.87ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count0ChemAxon
Hydrogen Donor Count0ChemAxon
Polar Surface Area0 ŲChemAxon
Rotatable Bond Count0ChemAxon
Refractivity17.47 m³·mol⁻¹ChemAxon
Polarizability9.36 ųChemAxon
Number of Rings0ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleYesChemAxon
MDDR-like RuleYesChemAxon
Spectra
Spectra
Spectrum TypeDescriptionSplash KeyDeposition DateView
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 10V, Positivesplash10-014i-0900000000-2cdcb21e78caf03fed282019-02-23View Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 20V, Positivesplash10-014i-0900000000-4a32f3d972a1268e00c22019-02-23View Spectrum
Predicted LC-MS/MSPredicted LC-MS/MS Spectrum - 40V, Positivesplash10-014i-3900000000-8dc259c15dc1c82eb0de2019-02-23View Spectrum
Toxicity Profile
Route of ExposureOral (12) ; inhalation (12) ; dermal (12)
Mechanism of ToxicityOnce in the body, beryllium acts as a hapten and interacts with human leucocyte antigen (HLA) DP presenting cells in the lungs, becoming physically associated with a major histocompatability (MHC) class II molecule. This MHC class II-beryllium-peptide complex is recognized by the T lymphocyte receptor, triggering CD4+ T lymphocyte activation and proliferation. The resulting inflammatory response is a cell-mediated process orchestrated by cytokines and results in the formation of (usually pulmonary) granulomas. Beryllium's toxicity may be controlled by the iron-storage protein ferritin, which sequesters beryllium by binding it and preventing it from interacting with other enzymes. Bromine is a powerful oxidizing agent and is able to release oxygen free radicals from the water in mucous membranes. These free radicals are also potent oxidizers and produce tissue damage. In additon, the formation of hydrobromic and bromic acids will result in secondary irritation. The bromide ion is also known to affect the central nervous system, causing bromism. This is believed to be a result of bromide ions substituting for chloride ions in the in actions of neurotransmitters and transport systems, thus affecting numerous synaptic processes. (12, 13, 3, 8, 1, 2)
MetabolismBeryllium is absorbed mainly through the lungs, where it enters the bloodstream and is transported throughout the body by binding to prealbumins and gamma-globulins. Beryllium accumulates in lung tissue and the skeleton. It is excreted mainly in the urine. Bromine is mainly absorbed via inhalation, but may also enter the body through dermal contact. Bromine salts can be ingested. Due to its reactivity, bromine quickly forms bromide and may be deposited in the tissues, displacing other halogens. (12, 8)
Toxicity ValuesNot Available
Lethal DoseNot Available
Carcinogenicity (IARC Classification)1, carcinogenic to humans. (10)
Uses/SourcesBeryllium foil is used in x-ray lithography for making integrated circuits. It is used as a reflector or moderator in nuclear reactions. Beryllium is used in gyroscopes and computer parts. Beryllium bromide has been used as a catalyst for the bromination of several organic molecules (14, 4).
Minimum Risk LevelChronic Oral: 0.002 mg/kg/day (Beryllium) (9)
Health EffectsAcute inhalation of a high level of beryllium can result in a pneumonia-like condition called acute beryllium disease. Chronic inhalation of beryllium can cause an inflammatory reaction in the respiratory system called chronic beryllium disease. Chronic beryllium disease may result in anorexia and weight loss, as well as right side heart enlargement and heart disease in advanced cases. Chronic exposure can also increase the risk of lung cancer. Skin contact with beryllium results in contact dermatitus. Bromine vapour causes irritation and direct damage to the mucous membranes. Elemental bromine also burns the skin. The bromide ion is a central nervous system depressant and chronic exposure produces neuronal effects. This is called bromism and can result in central reactions reaching from somnolence to coma, cachexia, exicosis, loss of reflexes or pathologic reflexes, clonic seizures, tremor, ataxia, loss of neural sensitivity, paresis, papillar edema of the eyes, abnormal speech, cerebral edema, delirium, aggressiveness, and psychoses. (11, 12, 13, 7, 8)
SymptomsChronic beryllium disease causes fatigue, weakness, difficulty breathing, and a persistent dry cough. Bromine vapour causes irritation and direct damage to the mucous membranes. Symptoms include lacrimation, rhinorrhoea, eye irritation with mucous secretions from the oropharyngeal and upper airways, coughing, dyspnoea, choking, wheezing, epistaxis, and headache. The bromide ion is a central nervous system depressant producing ataxia, slurred speech, tremor, nausea, vomiting, lethargy, dizziness, visual disturbances, unsteadiness, headaches, impaired memory and concentration, disorientation and hallucinations. This is called bromism. (12, 13, 7, 8)
TreatmentEYES: 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.
Normal Concentrations
Not Available
Abnormal Concentrations
Not Available
DrugBank IDNot Available
HMDB IDNot Available
PubChem Compound ID82230
ChEMBL IDNot Available
ChemSpider ID74208
KEGG IDNot Available
UniProt IDNot Available
OMIM ID
ChEBI IDNot Available
BioCyc IDNot Available
CTD IDNot Available
Stitch IDBeryllium bromide
PDB IDNot Available
ACToR IDNot Available
Wikipedia LinkNot Available
References
Synthesis ReferenceNot Available
MSDSNot Available
General References
  1. Amicosante M, Berretta F, Dweik R, Saltini C: Role of high-affinity HLA-DP specific CLIP-derived peptides in beryllium binding to the HLA-DPGlu69 berylliosis-associated molecules and presentation to beryllium-sensitized T cells. Immunology. 2009 Sep;128(1 Suppl):e462-70. doi: 10.1111/j.1365-2567.2008.03000.x. Epub 2008 Dec 23. [19191908 ]
  2. Lindenschmidt RC, Sendelbach LE, Witschi HP, Price DJ, Fleming J, Joshi JG: Ferritin and in vivo beryllium toxicity. Toxicol Appl Pharmacol. 1986 Feb;82(2):344-50. [3945960 ]
  3. Ziouzenkova O, Orasanu G, Sharlach M, Akiyama TE, Berger JP, Viereck J, Hamilton JA, Tang G, Dolnikowski GG, Vogel S, Duester G, Plutzky J: Retinaldehyde represses adipogenesis and diet-induced obesity. Nat Med. 2007 Jun;13(6):695-702. Epub 2007 May 27. [17529981 ]
  4. REED LJ, DeBUSK BG, GUNSALUS IC, HORNBERGER CS Jr: Crystalline alpha-lipoic acid; a catalytic agent associated with pyruvate dehydrogenase. Science. 1951 Jul 27;114(2952):93-4. [14854913 ]
  5. Golomb, BA (1999). A Review of the Scientific Literature As It Pertains to Gulf War Illnesses. Volume 2: Pyridostigmine Bromide. Washington, DC: RAND.
  6. Emeleus HJ and Sharpe AG (1972). (Advances in Inorganic Chemistry and Radiochemistry. Vol 14. New York, NY: Academic Press.
  7. Wikipedia. Beryllium. Last Updated 17 March 2009. [Link]
  8. ATSDR - Agency for Toxic Substances and Disease Registry (2002). Toxicological profile for beryllium. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]
  9. 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]
  10. International Agency for Research on Cancer (2014). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. [Link]
  11. Wikipedia. Bromine. Last Updated 9 June 2009. [Link]
  12. International Programme on Chemical Safety (IPCS) INCHEM (1992). Poison Information Monograph for Bromine. [Link]
  13. Wikipedia. Potassium bromide. Last Updated 9 June 2009. [Link]
  14. About.com: Chemstry (2009). Beryllium Facts. [Link]
Gene Regulation
Up-Regulated GenesNot Available
Down-Regulated GenesNot Available

Targets

General Function:
Voltage-gated chloride channel activity
Specific Function:
Voltage-gated chloride channel. Chloride channels have several functions including the regulation of cell volume; membrane potential stabilization, signal transduction and transepithelial transport.
Gene Name:
CLCN1
Uniprot ID:
P35523
Molecular Weight:
108625.435 Da
References
  1. Simchowitz L: Interactions of bromide, iodide, and fluoride with the pathways of chloride transport and diffusion in human neutrophils. J Gen Physiol. 1988 Jun;91(6):835-60. [3047312 ]
  2. Pusch M, Jordt SE, Stein V, Jentsch TJ: Chloride dependence of hyperpolarization-activated chloride channel gates. J Physiol. 1999 Mar 1;515 ( Pt 2):341-53. [10050002 ]
General Function:
Voltage-gated chloride channel activity
Specific Function:
Voltage-gated chloride channel. Chloride channels have several functions including the regulation of cell volume; membrane potential stabilization, signal transduction and transepithelial transport. May be important in urinary concentrating mechanisms.
Gene Name:
CLCNKA
Uniprot ID:
P51800
Molecular Weight:
75284.08 Da
References
  1. Simchowitz L: Interactions of bromide, iodide, and fluoride with the pathways of chloride transport and diffusion in human neutrophils. J Gen Physiol. 1988 Jun;91(6):835-60. [3047312 ]
  2. Pusch M, Jordt SE, Stein V, Jentsch TJ: Chloride dependence of hyperpolarization-activated chloride channel gates. J Physiol. 1999 Mar 1;515 ( Pt 2):341-53. [10050002 ]
General Function:
Voltage-gated chloride channel activity
Specific Function:
Voltage-gated chloride channel. Chloride channels have several functions including the regulation of cell volume; membrane potential stabilization, signal transduction and transepithelial transport. May be important in urinary concentrating mechanisms.
Gene Name:
CLCNKB
Uniprot ID:
P51801
Molecular Weight:
75445.3 Da
References
  1. Simchowitz L: Interactions of bromide, iodide, and fluoride with the pathways of chloride transport and diffusion in human neutrophils. J Gen Physiol. 1988 Jun;91(6):835-60. [3047312 ]
  2. Pusch M, Jordt SE, Stein V, Jentsch TJ: Chloride dependence of hyperpolarization-activated chloride channel gates. J Physiol. 1999 Mar 1;515 ( Pt 2):341-53. [10050002 ]
General Function:
Peptide antigen binding
Specific Function:
Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II loading compartments. In addition to APCs, other cells of the gastrointestinal tract, such as epithelial cells, express MHC class II molecules and CD74 and act as APCs, which is an unusual trait of the GI tract. To produce a MHC class II molecule that presents an antigen, three MHC class II molecules (heterodimers of an alpha and a beta chain) associate with a CD74 trimer in the ER to form a heterononamer. Soon after the entry of this complex into the endosomal/lysosomal system where antigen processing occurs, CD74 undergoes a sequential degradation by various proteases, including CTSS and CTSL, leaving a small fragment termed CLIP (class-II-associated invariant chain peptide). The removal of CLIP is facilitated by HLA-DM via direct binding to the alpha-beta-CLIP complex so that CLIP is released. HLA-DM stabilizes MHC class II molecules until primary high affinity antigenic peptides are bound. The MHC II molecule bound to a peptide is then transported to the cell membrane surface. In B-cells, the interaction between HLA-DM and MHC class II molecules is regulated by HLA-DO. Primary dendritic cells (DCs) also to express HLA-DO. Lysosomal microenvironment has been implicated in the regulation of antigen loading into MHC II molecules, increased acidification produces increased proteolysis and efficient peptide loading.
Gene Name:
HLA-DPA1
Uniprot ID:
P20036
Molecular Weight:
29380.345 Da
References
  1. Amicosante M, Berretta F, Dweik R, Saltini C: Role of high-affinity HLA-DP specific CLIP-derived peptides in beryllium binding to the HLA-DPGlu69 berylliosis-associated molecules and presentation to beryllium-sensitized T cells. Immunology. 2009 Sep;128(1 Suppl):e462-70. doi: 10.1111/j.1365-2567.2008.03000.x. Epub 2008 Dec 23. [19191908 ]
  2. ATSDR - Agency for Toxic Substances and Disease Registry (2002). Toxicological profile for beryllium. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]
General Function:
Peptide antigen binding
Specific Function:
Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II loading compartments. In addition to APCs, other cells of the gastrointestinal tract, such as epithelial cells, express MHC class II molecules and CD74 and act as APCs, which is an unusual trait of the GI tract. To produce a MHC class II molecule that presents an antigen, three MHC class II molecules (heterodimers of an alpha and a beta chain) associate with a CD74 trimer in the ER to form a heterononamer. Soon after the entry of this complex into the endosomal/lysosomal system where antigen processing occurs, CD74 undergoes a sequential degradation by various proteases, including CTSS and CTSL, leaving a small fragment termed CLIP (class-II-associated invariant chain peptide). The removal of CLIP is facilitated by HLA-DM via direct binding to the alpha-beta-CLIP complex so that CLIP is released. HLA-DM stabilizes MHC class II molecules until primary high affinity antigenic peptides are bound. The MHC II molecule bound to a peptide is then transported to the cell membrane surface. In B-cells, the interaction between HLA-DM and MHC class II molecules is regulated by HLA-DO. Primary dendritic cells (DCs) also to express HLA-DO. Lysosomal microenvironment has been implicated in the regulation of antigen loading into MHC II molecules, increased acidification produces increased proteolysis and efficient peptide loading.
Gene Name:
HLA-DPB1
Uniprot ID:
P04440
Molecular Weight:
29159.195 Da
References
  1. Amicosante M, Berretta F, Dweik R, Saltini C: Role of high-affinity HLA-DP specific CLIP-derived peptides in beryllium binding to the HLA-DPGlu69 berylliosis-associated molecules and presentation to beryllium-sensitized T cells. Immunology. 2009 Sep;128(1 Suppl):e462-70. doi: 10.1111/j.1365-2567.2008.03000.x. Epub 2008 Dec 23. [19191908 ]
  2. ATSDR - Agency for Toxic Substances and Disease Registry (2002). Toxicological profile for beryllium. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]
General Function:
Peptide antigen binding
Specific Function:
Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II loading compartments. In addition to APCs, other cells of the gastrointestinal tract, such as epithelial cells, express MHC class II molecules and CD74 and act as APCs, which is an unusual trait of the GI tract. To produce a MHC class II molecule that presents an antigen, three MHC class II molecules (heterodimers of an alpha and a beta chain) associate with a CD74 trimer in the ER to form a heterononamer. Soon after the entry of this complex into the endosomal/lysosomal system where antigen processing occurs, CD74 undergoes a sequential degradation by various proteases, including CTSS and CTSL, leaving a small fragment termed CLIP (class-II-associated invariant chain peptide). The removal of CLIP is facilitated by HLA-DM via direct binding to the alpha-beta-CLIP complex so that CLIP is released. HLA-DM stabilizes MHC class II molecules until primary high affinity antigenic peptides are bound. The MHC II molecule bound to a peptide is then transported to the cell membrane surface. In B-cells, the interaction between HLA-DM and MHC class II molecules is regulated by HLA-DO. Primary dendritic cells (DCs) also to express HLA-DO. Lysosomal microenvironment has been implicated in the regulation of antigen loading into MHC II molecules, increased acidification produces increased proteolysis and efficient peptide loading.
Gene Name:
HLA-DPB1
Uniprot ID:
P04440
Molecular Weight:
29159.195 Da
References
  1. Amicosante M, Berretta F, Dweik R, Saltini C: Role of high-affinity HLA-DP specific CLIP-derived peptides in beryllium binding to the HLA-DPGlu69 berylliosis-associated molecules and presentation to beryllium-sensitized T cells. Immunology. 2009 Sep;128(1 Suppl):e462-70. doi: 10.1111/j.1365-2567.2008.03000.x. Epub 2008 Dec 23. [19191908 ]
  2. ATSDR - Agency for Toxic Substances and Disease Registry (2002). Toxicological profile for beryllium. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]
General Function:
Inhibitory extracellular ligand-gated ion channel activity
Specific Function:
Component of the heteropentameric receptor for GABA, the major inhibitory neurotransmitter in the vertebrate brain. Functions also as histamine receptor and mediates cellular responses to histamine. Functions as receptor for diazepines and various anesthetics, such as pentobarbital; these are bound at a separate allosteric effector binding site. Functions as ligand-gated chloride channel (By similarity).
Gene Name:
GABRA1
Uniprot ID:
P14867
Molecular Weight:
51801.395 Da
References
  1. Suzuki S, Kawakami K, Nakamura F, Nishimura S, Yagi K, Seino M: Bromide, in the therapeutic concentration, enhances GABA-activated currents in cultured neurons of rat cerebral cortex. Epilepsy Res. 1994 Oct;19(2):89-97. [7843172 ]
General Function:
Gaba-gated chloride ion channel activity
Specific Function:
Component of the heteropentameric receptor for GABA, the major inhibitory neurotransmitter in the vertebrate brain. Functions also as histamine receptor and mediates cellular responses to histamine. Functions as receptor for diazepines and various anesthetics, such as pentobarbital; these are bound at a separate allosteric effector binding site. Functions as ligand-gated chloride channel.
Gene Name:
GABRB3
Uniprot ID:
P28472
Molecular Weight:
54115.04 Da
References
  1. Suzuki S, Kawakami K, Nakamura F, Nishimura S, Yagi K, Seino M: Bromide, in the therapeutic concentration, enhances GABA-activated currents in cultured neurons of rat cerebral cortex. Epilepsy Res. 1994 Oct;19(2):89-97. [7843172 ]
General Function:
Inhibitory extracellular ligand-gated ion channel activity
Specific Function:
Component of the heteropentameric receptor for GABA, the major inhibitory neurotransmitter in the vertebrate brain. Functions also as histamine receptor and mediates cellular responses to histamine. Functions as receptor for diazepines and various anesthetics, such as pentobarbital; these are bound at a separate allosteric effector binding site. Functions as ligand-gated chloride channel.
Gene Name:
GABRG2
Uniprot ID:
P18507
Molecular Weight:
54161.78 Da
References
  1. Suzuki S, Kawakami K, Nakamura F, Nishimura S, Yagi K, Seino M: Bromide, in the therapeutic concentration, enhances GABA-activated currents in cultured neurons of rat cerebral cortex. Epilepsy Res. 1994 Oct;19(2):89-97. [7843172 ]