1. 2-dichlorobenzene
2. O-dichlorobenzene
1. O-dichlorobenzene
2. 95-50-1
3. Ortho-dichlorobenzene
4. O-dichlorbenzol
5. 2-dichlorobenzene
6. Chloroben
7. Dilantin Db
8. Odcb
9. O-dichlorobenzol
10. Orthodichlorobenzol
11. Benzene, 1,2-dichloro-
12. Orthodichlorobenzene
13. Cloroben
14. Termitkil
15. Dizene
16. O-dichlorbenzene
17. Dowtherm E
18. Special Termite Fluid
19. Benzene, O-dichloro-
20. Dilatin Db
21. Dichlorobenzene, O-
22. 1,2-dichlorbenzene
23. Nci-c54944
24. 1,2 Dichlorobenzene
25. Dichlorobenzene Mixture
26. O-dcb
27. 1,2-dichloro-benzene
28. Nsc 60644
29. 25321-22-6
30. Odb
31. O-dichlor Benzol
32. 6pj93i88xl
33. Chloroden
34. Chebi:35290
35. Nsc-60644
36. 1219803-83-4
37. 1, 2-dichlorobenzene
38. Ncgc00090825-01
39. Dsstox_cid_430
40. Dsstox_rid_75581
41. Dsstox_gsid_20430
42. Caswell No. 301
43. Dichlorobenzenes
44. Cas-95-50-1
45. Dichlorobenzene, Ortho, Liquid
46. Ccris 1360
47. Hsdb 521
48. Einecs 202-425-9
49. Un1591
50. Rcra Waste No. U070
51. Epa Pesticide Chemical Code 059401
52. Unii-6pj93i88xl
53. 1,2-dichlorobenzene (o-dichlorobenzene)
54. O-dichlorobezene
55. Ai3-00053
56. 0-dichlorobenzene
57. O-dichlrorobenzene
58. O-dichloro Benzene
59. O-dichloro-benzene
60. 1,2-dichlorobenzen
61. Ortho Dichlorobenzene
62. Mfcd00000535
63. 1,2-dichiorobenzene
64. 1.2-dichlorobenzene
65. 2,3-dichlorobenzene
66. 3,4-dichlorobenzene
67. Benzene,2-dichloro-
68. Dichlorobenzene, Ortho
69. 1 ,2-dichlorobenzene
70. 1, 2 Dichlorobenzene
71. 1,2-dichlor-obenzene
72. 1,2-dichloro Benzene
73. 1,2-di-chlorobenzene
74. Wln: Gr Bg
75. 1,2-bis(chloranyl)benzene
76. Ec 202-425-9
77. Schembl5190
78. Benzene,1,2-dichloro
79. Bidd:er0678
80. O-dichlorobenzene [mi]
81. Chembl298461
82. Dtxsid6020430
83. Zinc388506
84. Bcp08071
85. Nsc60644
86. Ortho-dichlorobenzene [hsdb]
87. Ortho-dichlorobenzene [iarc]
88. Orthodichlorobenzene [mart.]
89. Tox21_111030
90. Tox21_202157
91. Tox21_300046
92. 1-bromo-3,5-dichlorobenzene-[d3]
93. Stl283948
94. 1,2-dichlorobenzene, Lr, >=98%
95. Akos000120142
96. 1,2-dichlorobenzene, Anhydrous, 99%
97. Am87481
98. Db13963
99. Gf-0116
100. Un 1591
101. 1,2-dichlorobenzene, For Hplc, 99%
102. Ncgc00090825-02
103. Ncgc00090825-03
104. Ncgc00253914-01
105. Ncgc00259706-01
106. 1,2-dichlorobenzene Ortho-dichlorobenzene
107. 1,3-cyclohexadien-5-yne,1,2-dichloro-
108. Bp-31152
109. 95-50-125321-22-6(mixedisomers)
110. Db-045754
111. 1,2-dichlorobenzene, Reagentplus(r), 99%
112. D1116
113. Ft-0606382
114. Ft-0606383
115. S0668
116. 1,2-dichlorobenzene, For Synthesis, 99.0%
117. 1,2-dichlorobenzene 100 Microg/ml In Methanol
118. A845316
119. J-503814
120. Q2609815
121. O-dichlorobenzene [un1591] [keep Away From Food]
122. 1,2-dichlorobenzene, Pestanal(r), Analytical Standard
123. F1908-0113
124. 1,2-dichlorobenzene Solution, Certified Reference Material, 200 Mug/ml In Methanol
125. 1,2-dichlorobenzene Solution, Certified Reference Material, 5000 Mug/ml In Methanol
126. 1,2-dichlorobenzene Solution, Nmr Reference Standard, 1% In Acetone-d6 (99.9 Atom % D), Nmr Tube Size 3 Mm X 8 In.
127. 1,2-dichlorobenzene Solution, Nmr Reference Standard, 5% In Acetone-d6 (99.9 Atom % D), Nmr Tube Size 5 Mm X 8 In.
128. Yan
| Molecular Weight | 147.00 g/mol |
|---|---|
| Molecular Formula | C6H4Cl2 |
| XLogP3 | 3.4 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 0 |
| Rotatable Bond Count | 0 |
| Exact Mass | 145.9690055 g/mol |
| Monoisotopic Mass | 145.9690055 g/mol |
| Topological Polar Surface Area | 0 Ų |
| Heavy Atom Count | 8 |
| Formal Charge | 0 |
| Complexity | 62.9 |
| 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 |
Insecticides
Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics. (See all compounds classified as Insecticides.)
Urine samples collected from 8 volunteers for 36 hr after exposure to 1,2-DCB in the range of 0.03-0.3 mg/L and, in one case up to 0.54 mg/L for two 4 hr periods with a 45 min interval were analysed for the presence of isomeric dichlorophenylmercapturic acids; ethyl esters of 2,3-dichlorophenylmercapturic acid and 3,4-dichlorophenylmercapturic acid were detected in the urine, with a linear correlation found between urinary dichlorophenylmercapturic acid concentration and the level of 1,2-DCB exposure; a first-order excretion kinetic was determined for the two dichlorophenylmercapturic acids; the half lives of 3,4-dichlorophenylmercapturic acid and 2,3-dichlorophenylmercapturic acid were determined to be 5.9 +/- 1.7 hr and 5.3 +/- 3.0 hr respectively.
Organization for Economic Cooperation and Development; Screening Information Data Set for 1,2-Dichlorobenzene, 95-50-1 p.181 (November 6-9, 2001). Available from, as of February 7, 2008: https://www.chem.unep.ch/irptc/sids/OECDSIDS/sidspub.html
The dichlorobenzenes may be absorbed through the lung, gastrointestinal tract, and intact skin. Relatively low water solubility and high lipid solubility favor their penetration of most membranes by diffusion, including pulmonary and GI epithelia, the brain, hepatic parenchyma, renal tubules, and the placenta. /Dichlorobenzenes/
USEPA; Ambient Water Quality Criteria Doc: Dichlorobenzenes p.C-14 (1980) EPA 440/5-80-039
The relationship between the metabolism and the toxicity of ortho-dichlorobenzene was investigated by evaluating its biotransformation, tissue distribution, blood kinetics and excretion after oral administration of 5, 50 or 250 mg/kg bw to male Wistar rats. The dose of 250 mg/kg bw had been demonstrated to be toxic in previous studies. The major route of elimination of ortho-dichlorobenzene (75-85%) was via the kidneys; excretion in the feces represented 19% of the low dose and 7% of the high dose. Excretion was nearly complete within 24 hr after the low and intermediate doses and within 48 hr after the high dose. Pretreatment with phenobarbital accelerated excretion of the high dose and resulted in an overall higher proportion of urinary excretion. Biliary excretion constituted 50-60% of the dose, indicating significant enterohepatic recirculation. The highest concentrations of radiolabel after a low dose were found in fat, liver and kidney 6 hr after administration; these then declined rapidly. The maximal concentration in blood was reached 6-8 hr after administration of the low and intermediate doses and 24 hr after the high dose. ortho-Dichlorobenzene was detected in blood only during the first 2 hr after administration of 5 mg/kg bw. The major route of biotransformation was via the glutathione pathway, 60% of the urinary metabolites being mercapturic acids; the major metabolites in bile were also conjugates of glutathione. Other major metabolites in urine were the sulfate conjugates of 2,3- and 3,4- dichlorophenol. No significant differences in metabolic profiles were observed with dose. Induction with phenobarbital increased excretion of sulfate conjugates (30% in induced rats, 20% in control rats), the main one being the conjugate of 3,4-dichlorophenol. The mercapturic acids in urine and the glutathione conjugates in bile were epoxide-derived metabolites, and no quinone- or hydroquinone-derived metabolites were observed. A high dose of ortho-dichlorobenzene results in depletion of glutathione, followed by oxidative stress and possibly binding to macromolecules.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V73 242 (1999)
1,2-Dichlorobenzene is well absorbed via the oral route. In rats, absorption of 1,2-dichlorobenzene from the gastrointestinal tract was considered complete at doses of 5 and 50 mg/kg bw but incomplete (83% absorption) at 250 mg/kg bw. There are no quantitative data for the dermal and inhalation absorption of 1,2-dichlorobenzene in animals or absorption of the chemical via any route in humans. Studies with rats have shown that 1,2-dichlorobenzene is distributed primarily to the adipose tissue with lesser amounts detected in the kidneys, liver and plasma. 1,2-Dichlorobenzene equivalents were bound to the kidneys, liver and plasma with covalent binding accounting for a substantial proportion of bound material. In particular, ...non-specific covalent binding to the alpha2u-globulin fraction of the rat kidney /was observed/. Several studies have found that the administration of a single dose of 1,2-dichlorobenzene by either the oral, intraperitoneal or intravenous route results in high initial tissue levels of 1,2-dichlorobenzene equivalents. Peak tissue levels occur within 1 and 6 hours, depending on the method of administration, followed by rapid decline thereafter
Organization for Economic Cooperation and Development; Screening Information Data Set for 1,2-Dichlorobenzene, 95-50-1 p.21 (November 6-9, 2001). Available from, as of January 31, 2008: https://www.chem.unep.ch/irptc/sids/OECDSIDS/sidspub.html
For more Absorption, Distribution and Excretion (Complete) data for 1,2-DICHLOROBENZENE (9 total), please visit the HSDB record page.
2,3- and 3,4-Dichlorophenyl methyl sulfoxides and 2,3- and 3,4-dichlorophenyl methyl sulfones (2,3- and 3,4-DCPSO2Mes) were detected in the urine of rats administered o-dichlorobenzene (o-DCB). After administration of o-DCB to rats, swift decreases were observed in the concentrations of o-DCB in blood, liver, and kidneys, whereas 3,4-DCPSO2Me appeared in blood, liver, kidneys, and adipose tissue. The concentrations of 3,4-DCPSO2Me in the blood and three tissues reached maxima at 24 hr. Both aminopyrine N-demethylase and aniline hydroxylase activities and cytochrome P450 content of hepatic microsomes decreased 24 hr after administration of o-DCB. In contrast, 3,4-DCPSO2Me increased the activities of these enzymes and cytochrome P450 and b5 contents in rat liver microsomes. In both antibiotic-pretreated and bile duct-cannulated rats dosed with o-DCB, the concentrations of 2,3- and 3,4-DCPSO2Mes in blood, liver, kidneys, and adipose tissue were dramatically reduced. These findings suggest that the process of formation of methylsulfonyl metabolites of o-DCB involves biliary secretion of DCPSO2Mes and/or their precursors which will be subjected to metabolism by intestinal microflora. In antibiotic-pretreated rats, the inhibitory effects of o-DCB administration on the activities of aminopyrine- and aniline-metabolizing enzymes and the contents of cytochromes P450 and b5 in hepatic microsomes were greater than those observed in the intact rats. In bile duct-cannulated rats, the decrease in aminopyrine N-demethylase activity after administration of o-DCB was greater than that observed in the intact rats. These findings suggest that the apparent inhibition of drug-metabolizing enzymes by o-DCB is the result of simultaneous contrary effects, namely, the inductive effect of 3,4-DCPSO2Me and the stronger inhibitory effect of an unknown factor(s) on drug-metabolizing enzymes.
PMID:9266800 Kato Y, Kimura R: Toxicol Appl Pharmacol 145 (2): 277-84 (1997)
After ingestion of o-dichlorobenzene, urine of rabbits was found to contain 2,3- and 3,4-dichlorophenol free and o-glucuronic and sulfuric acid conjugates, 3,4- and 4,5-dichlorocatechol free and as the o-glucuronide and sulfate, and 3,4-dichlorophenylmercapturic acid.
Menzie, C.M. Metabolism of Pesticides. U.S. Department of the Interior, Bureau of Sport Fisheries and Wildlife, Publication 127. Washington, DC: U.S. Government Printing Office, 1969., p. 155
The effect of inducers and inhibitors of microsomal mixed-function oxidases on the fate of metabolism and the extent of binding of ortho- and para-dichlorobenzene to cellular constituents suggests that arene oxides (epoxide) may be precursors of the excreted metabolites...
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V7 239 (1974)
o-Dichlorobenzene yielded N-acetyl-S-(3,4-dichlorophenoxy)-L-cysteine in rabbits. /from table/
Goodwin, B.L. Handbook of Intermediary Metabolism of Aromatic Compounds. New York: Wiley, 1976., p. D-15
For more Metabolism/Metabolites (Complete) data for 1,2-DICHLOROBENZENE (15 total), please visit the HSDB record page.
1,2-dichlorobenzene has known human metabolites that include 2,3-dichlorophenol and 3,4-dichlorophenol.
S73 | METXBIODB | Metabolite Reaction Database from BioTransformer | DOI:10.5281/zenodo.4056560
...Estimated half-life of 1,2-DCB was 0.08, 0.04 and 0.02 hours for blood, liver and kidney respectively in male Wistar rats given 1.36 mmol/kg (200 mg/kg bw) ip.
Organization for Economic Cooperation and Development; Screening Information Data Set for 1,2-Dichlorobenzene, 95-50-1 p.172 (November 6-9, 2001). Available from, as of February 7, 2008: https://www.chem.unep.ch/irptc/sids/OECDSIDS/sidspub.html
1,2-dichlorobenzene (1,2-DCB), an industrial solvent, is a known hepatotoxicant. Two oxidative events in the liver contribute to 1,2-DCB-induced liver injury: an initial hepatocellular oxidative stress, followed by oxidant stress associated with an inflammatory response. We hypothesize that the initial hepatocellular oxidative event triggers molecular and cellular processes within hepatocytes that lead to the production of factors that contribute to Kupffer cell (KC) activation and upregulation of the inflammatory cascade. To investigate the molecular effects of 1,2-DCB, primary cultures of Fischer-344 (F-344) and Sprague-Dawley (SD) rat hepatocytes were incubated with 1,2-DCB (3.6-12.4 umol) and examined for enhanced DNA-binding activity of the oxidant-sensitive transcription factors activator protein-1 (AP-1), nuclear factor-kappa B (NF-kappaB), and electrophile responsive element (EpRE), and production and release of the chemokine cytokine-induced neutrophil chemoattractant (CINC). In F-344 rat hepatocytes, the activities of AP-1 and NF-kappaB were increased by as much as 3-fold by 6 h of 1,2-DCB treatment, when compared to control. Nuclear translocation of EpRE was also enhanced by 3-fold and occurred 2 h following 1,2-DCB treatment. These events were greater in F-344 than in SD rat hepatocytes incubated with 1,2-DCB. Moreover, F-344 rat hepatocytes produced and released CINC following incubation with 1,2-DCB, but SD rat hepatocytes did not. Lastly, conditioned media from 1,2-DCB-treated F-344 rat hepatocytes stimulated KC activity as determined by enhanced NF-kappaB-binding activity and increased nitric oxide production. Collectively, these data suggest that the mechanisms of 1,2-DCB-induced hepatotoxicity involve intercellular communication whereby compromised hepatocytes may signal KC activation via the production and release of oxidant-sensitive chemokines and cytokines.
PMID:12915711 Younis HS et al; Toxicol Sci 76 (1): 201-11 (2003)
... Although, hepatotoxic injury of o-DCB is greater in Fischer 344 (F344) when compared with Sprague Dawley (S-D) rats, this interstrain difference does not transcend into any difference in lethal effects of o-DCB. Interstrain difference in compensatory tissue repair has been suggested as the underlying mechanism for the lack of strain differences in lethality ... The objectives of the present study were (1) to investigate if the differences in compensatory tissue repair are reflected in differential protooncogene expression in S-D versus F344 rat livers and (2) to investigate if changes in protooncogene expression could explain the decrease and delay in tissue repair response beyond a threshold of 0.6 mL o-DCB/kg. Male S-D and F344 rats (8/9 weeks old) were administered either 0.6 or 1.2 mL o-DCB/kg and changes in expression of protooncogenes c-myc (immediate early) and Ha-ras (delayed early) were examined over a time course. Findings of this study indicate that the timing and extent of c-myc and Ha-ras expression varies in the two strains following administration of o-DCB. ...
PMID:10614693 Kulkarni SG et al; Toxicology 129; 139 (1-2): 119-27 (1999)
The more pronounced toxicity to the liver of the ortho-isomer has been associated with a more pronounced binding of the compound or its intermediate metabolites to liver proteins...
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V7 239 (1974)
para-Dichlorobenzene, but not ortho-dichlorobenzene, induces renal tumors specifically in male rats. There is substantial evidence that para-dichlorobenzene induces these tumors through an alpha2u-globulin-associated response. Although para-dichlorobenzene does not bind to DNA in the male rat kidney, there is weak evidence that it binds to DNA in several tissues in treated mice. Both ortho- and para-dichlorobenzene have been reported to bind to proteins and DNA in the same mouse tissues. No attempt was made to isolate any DNA adducts. The data available on the genotoxicity of para-dichlorobenzene and ortho-dichlorobenzene also do not allow any distinction to be made between these two compounds, which differ significantly in their tumorigenicity: ortho-dichlorobenzene does not cause tumors, whereas para-dichlorobenzene causes liver tumors in mice and kidney tumors in male rats. Overall, the data on genotoxicity do not support a mechanism for renal-cell tumor induction in rats involving direct interaction of para-dichlorobenzene with DNA. Therefore, the overall data, including those on genotoxicity, indicate that para-dichlorobenzene causes renal tumors in male rats through an alpha2u-globulin associated response.
IARC. Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans. Geneva: World Health Organization, International Agency for Research on Cancer, 1972-PRESENT. (Multivolume work). Available at: https://monographs.iarc.fr/ENG/Classification/index.php, p. V73 262 (1999)
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