1. Bromobenzene, 14c-labeled
1. 108-86-1
2. Phenyl Bromide
3. Monobromobenzene
4. Benzene, Bromo-
5. 1-bromobenzene
6. Phbr
7. Nci-c55492
8. C6h5br
9. Bromo-benzene
10. 4-bromobenzene
11. Bromobenzol
12. Hsdb 47
13. Phenylbromide
14. Ccris 5887
15. Nsc 6529
16. Einecs 203-623-8
17. Unii-co4d5j547l
18. Chebi:3179
19. Co4d5j547l
20. Dtxsid5024637
21. Ai3-09059
22. Nsc-6529
23. Dtxcid304637
24. Bromobenzene 100 Microg/ml In Methanol
25. Bromo Benzene
26. Mfcd00000056
27. Smr000112021
28. Un2514
29. Bromanylbenzene
30. Brombenzene
31. Brombenzol
32. Bromobezene
33. 3-bromobenzene
34. 2-bromobenzene
35. 1-bromo-benzene
36. 1-bromobenzene; Bromobenzene; Bromobenzol; Monobromobenzene; Nsc 6529; Phenyl Bromide
37. Bromobenzene--d4
38. Mfcd00000055
39. 64646-03-3
40. Bromobenzene [mi]
41. Bromobenzene [un2514] [flammable Liquid]
42. Wln: Er
43. Bromobenzene [hsdb]
44. Schembl1542
45. Mls000515541
46. Mls002415720
47. Bromobenzene, Lr, >=99%
48. Chembl16068
49. Bromobenzene, Analytical Standard
50. Nsc6529
51. Bromobenzene, >=99.5% (gc)
52. Hms2269p12
53. Bcp26654
54. Bcp30008
55. Str00651
56. Tox21_200849
57. Br1026
58. Bromobenzene, Reagentplus(r), 99%
59. Stl264221
60. Bromobenzene, For Synthesis, 99.5%
61. Akos000120123
62. Un 2514
63. Ncgc00091842-01
64. Ncgc00091842-02
65. Ncgc00091842-03
66. Ncgc00091842-04
67. Ncgc00258403-01
68. Cas-108-86-1
69. Sy061516
70. B0439
71. Ft-0617692
72. Ft-0617909
73. Ft-0623223
74. En300-19359
75. A801934
76. Q410597
77. Bromo(2h5)benzene Pound>>pentadeuterophenyl Bromide
78. J-002199
79. J-519941
80. F1908-0102
81. Inchi=1/c6h5br/c7-6-4-2-1-3-5-6/h1-5
| Molecular Weight | 157.01 g/mol |
|---|---|
| Molecular Formula | C6H5Br |
| XLogP3 | 3 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 0 |
| Rotatable Bond Count | 0 |
| Exact Mass | g/mol |
| Monoisotopic Mass | g/mol |
| Topological Polar Surface Area | 0 |
| Heavy Atom Count | 7 |
| Formal Charge | 0 |
| Complexity | 46.1 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 0 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 0 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
4 (?). 4= VERY TOXIC: PROBABLE ORAL LETHAL DOSE (HUMAN) IS 50-500 MG/KG, BETWEEN 1 TEASPOON & 1 OUNCE FOR 70 KG PERSON (150 LB).
Gosselin, R.E., H.C. Hodge, R.P. Smith, and M.N. Gleason. Clinical Toxicology of Commercial Products. 4th ed. Baltimore: Williams and Wilkins, 1976., p. II-114
50-500 mg/kg
ABSORBED THROUGH LUNGS, GI TRACT & INTACT SKIN. EXCRETED AS CATECHOL DERIVATIVES BOTH FREE & CONJUGATED WITH SULFATE OR MERCAPTURIC ACID.
Gosselin, R.E., H.C. Hodge, R.P. Smith, and M.N. Gleason. Clinical Toxicology of Commercial Products. 4th ed. Baltimore: Williams and Wilkins, 1976., p. II-114
BROMOBENZENE MAY BE METAB TO AN EPOXIDE...EXCRETED IN BILE, REABSORBED THROUGH ENTEROHEPATIC CIRCULATION, & METAB IN SEVERAL STEPS TO S-(P-BROMOPHENYL)MERCAPTURIC ACID, WHICH IS THEN EXCRETED IN URINE.
National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 693
This investigation was designed to determine whether biliary excretion of bromobenzene-glutathione conjugate can be used as an index of in vivo activation of bromobenzene. To test this hypothesis, the effect of chemicals known to alter the toxicity and biotransformation of bromobenzene (ie, cytochrome p450 inducers and inhibitors) on the biliary excretion of bromobenzene-glutathione was studied in rats. Bromobenzene-glutathione was the major bromobenzene metabolite in bile. A linear relationship was observed between the dosage of bromobenzene administered and bromobenzene-glutathione excreted into bile, up to a dosage of 250 umol/kg of bromobenzene. Of the inducers tested, Phenobarbital, which is known to increase the toxicity of bromobenzene, dramatically increased 1700 m1 the rate of biliary excretion of bromobenzene-glutathione over that in control animals. In contrast, 3-methylcholanthrene, which is known to decrease the hepatotoxicity of bromobenzene, decreased the biliary excretion of bromobenzene-glutathione (56%). Inhibitors of p450, such as SKF 525-A and piperonyl butoxide which are known to decrease the activation and hepatotoxicity of bromobenzene, also decreased the biliary excretion of bromobenzene-glutathione. These findings are in agreement with the hypothesis that the biliary excretion of bromobenzene-glutathione reflects the formation of the reactive bromobenzene metabolite in liver and the rate of biliary excretion can be used to determine factors that are important in determining the toxicity of bromobenzene.
Madhu C, Klaassen CD; Toxicol Lett (AMST) 60 (2): 227-36 (1992)
IT APPEARS THAT IN BROMOBENZENE NECROSIS /OF LIVER/, THE TOXIC /SRP: BROMOBENZENE EPOXIDE METABOLITES, MAINLY THE 3,4-EPOXIDE, ARE/...DEGRADED THROUGH THE ACTION OF GLUTATHIONE TRANSFERASE & EPOXIDE HYDRATASE.
Amdur, M.O., J. Doull, C.D. Klaasen (eds). Casarett and Doull's Toxicology. 4th ed. New York, NY: Pergamon Press, 1991., p. 346
BROMOBENZENE IS METABOLIZED VIA THE HEPATIC MIXED-FUNCTION OXIDASE SYSTEM TO REACTIVE INTERMEDIATES 2,3- AND 3,4-BROMOBENZENE EPOXIDES. THESE METABOLITES PRESUMABLY BIND TO TISSUE MACROMOLECULES. THE SPECIFIC SITES OF MACROMOLECULAR PROTEINS WERE INVESTIGATED. THE 3,4-EPOXIDE IS MORE REACTIVE, BINDING COVALENTLY TO MICROSOMAL PROTEIN AT THE SITE OF ITS SYNTHESIS, WHEREAS BROMOBENZENE 2,3-EPOXIDE IS MORE STABLE, LEAVING THE MICROSOMAL PROTEIN COMPARTMENT AND BINDING COVALENTLY TO SOL PROTEIN, IE THE HEMOGLOBIN BETA CHAIN.
PMID:7288634 LAU SS, ZANNONI VG; J PHARMACOL EXP THER 219 (2): 563 (1981)
BROMOBENZENE YIELDS N-ACETYL-S-(4-BROMO-1,2-DIHYDRO-2-HYDROXYPHENYL)-L-CYSTEINE IN RABBIT & RAT; N-ACETYL-S-(P-BROMOPHENYL)-L-CYSTEINE IN DOG & IN MOUSE. /FROM TABLE/
Goodwin, B.L. Handbook of Intermediary Metabolism of Aromatic Compounds. New York: Wiley, 1976., p. B-23
BROMOBENZENE MAY BE METABOLIZED TO AN EPOXIDE...EXCRETED IN BILE, REABSORBED THROUGH ENTEROHEPATIC CIRCULATION, & METABOLIZED IN SEVERAL STEPS TO S-P-BROMOPHENYL MERCAPTURIC ACID, WHICH IS THEN EXCRETED IN URINE.
National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 693
For more Metabolism/Metabolites (Complete) data for BROMOBENZENE (13 total), please visit the HSDB record page.
Bromobenzene is converted to either the 3,4-oxide derivative catalyzed primarily by phenobarbital-induced cytochrome isozymes (e.g., CYP 450 1A2, 2A6, 2B6, and 3A4), or the 2,3-oxide derivative catalyzed primarily by 3-methylcholanthrene and -naphthoflavone-induced CYP isozymes (e.g., CYP 450 1A1, 1A2, and 1B1). This is followed by urinary excretion as premercapturic and mercapturic acids.
FOLLOWING BROMOBENZENE (1.0 MMOL) ADMIN TO RAT HEPATOCYTES, LIPID PEROXIDATION OCCURRED ONLY AT A LATER STAGE, COMPARED TO TREATMENT WITH CCL4, AND ONLY AFTER CELL DEATH. APPARENTLY LIPID PEROXIDATION DURING BROMOBENZENE TOXICITY WAS MERELY A CONSEQUENCE OF GSH DEPLETION AND CELL DEATH. APPARENTLY, ARYLATION OF CRITICAL CELLULAR NUCLEOPHILES IS MORE IMPORTANT THAN LIPID PEROXIDATION IN BROMOBENZENE HEPATOTOXICITY.
PMID:6838624 SMITH MT ET AL; BIOCHEM PHARMACOL 32 (5): 763 (1983)
FRESHLY ISOLATED HEPATOCYTES FROM PHENOBARBITAL-TREATED RATS WERE INCUBATED IN THE PRESENCE OR ABSENCE OF EXTRACELLULAR CALCIUM WITH BROMOBENZENE. IN THE ABSENCE OF CALCIUM IT WAS FAR MORE TOXIC TO THE CELLS THAN IN ITS PRESENCE. THIS RESULT IS INCONSISTENT WITH THE HYPOTHESIS THAT AN INFLUX OF EXTRACELLULAR CALCIUM IS REQUIRED AS THE FINAL STEP IN TOXIC LIVER CELL INJURY.
SMITH MT ET AL; SCIENCE (WASH DC) 213 (4513): 1257 (1981)
A NOVEL METHOD IS DESCRIBED FOR MEASURING THE COVALENT BINDING OF BROMOBENZENE TO MACROMOLECULES IN RAT HEPATIC MICROSOMES OF HEPATOCYTES. COVALENT BINDING IN HEPATOCYTES SUGGESTS THAT THE BINDING OCCURS FIRST WITH MACROMOLECULES IN 20000-40000 DALTON RANGE.
DENT JG, SUN JD; ADV EXP MED BIOL 136A(BIOL REACT INTERMED-2, CHEM MECH BIOL EFF, PT A) 275 (1982)
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