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1. Aniline Aluminium Salt
2. Aniline Dihydrofluoride
3. Aniline Diphosphate (1:1)
4. Aniline Diphosphate (3:1)
5. Aniline Diphosphate (4:1)
6. Aniline Hydrobromide
7. Aniline Hydrochloride
8. Aniline Hydrochloride-(14)c-labeled Cpd
9. Aniline Hydrochloride-(15)n-labeled Cpd
10. Aniline Hydrofluoride
11. Aniline Hydrogen Iodide
12. Aniline Monosulfate
13. Aniline Nitrate
14. Aniline Perchlorate
15. Aniline Phosphate (1:1)
16. Aniline Phosphate (1:2)
17. Aniline Phosphate (2:1)
18. Aniline Phosphonate (1:1)
19. Aniline Sulfate
20. Aniline Sulfate (2:1)
21. Aniline Sulfate (2:1), (14)c-labeled Cpd
22. Aniline, (13)c-labeled Cpd
23. Aniline, (14)c-labeled Cpd
24. Aniline, 15n-labeled Cpd
25. Aniline, 2-(13)c-labeled Cpd
26. Aniline, 3-(13)c-labeled Cpd
27. Aniline, 3h-labeled Cpd
28. Aniline, 4-(13)c-labeled Cpd
29. Aniline, Conjugate Acid
30. Aniline, Ion(1+)
31. Aniline, Magnesium (1:1) Salt
32. Aniline, Monolithium Salt
33. Aniline, Sodium Salt
1. Benzenamine
2. 62-53-3
3. Phenylamine
4. Aminobenzene
5. Aminophen
6. Arylamine
7. Kyanol
8. Anilin
9. Cyanol
10. Aniline Oil
11. Benzeneamine
12. Benzidam
13. Krystallin
14. Anyvim
15. Blue Oil
16. Anilina
17. C.i. Oxidation Base 1
18. Huile D'aniline
19. Rcra Waste Number U012
20. C.i. 76000
21. Aniline Reagent
22. Nci-c03736
23. Un 1547
24. Chebi:17296
25. Mfcd00007629
26. Sir7xx2f1k
27. Benzene, Amino
28. Anilin [czech]
29. Ci Oxidation Base 1
30. Caswell No. 051c
31. Huile D'aniline [french]
32. Hsdb 43
33. Phenyleneamine
34. Anilinum
35. D'aniline
36. Rcra Waste No. U012
37. Anilina [italian, Polish]
38. Ccris 44
39. Aniline And Homologs
40. Aniline (and Salts)
41. Aniline And Homologues
42. Aniline Oil, Phenylamine
43. Einecs 200-539-3
44. Unii-sir7xx2f1k
45. Un1547
46. Epa Pesticide Chemical Code 251400
47. Benzenaminium
48. Cyanole
49. Ci 76000
50. Bidd:er0581
51. Phenyl Amine
52. Phenyl-amine
53. Ai3-03053
54. 8-aniline
55. Benzene, Amino-
56. Fentanyl Impurity F
57. 2-bromobenzylchloride
58. Aniline-[13c]
59. Phnh2
60. Anilinum [hpus]
61. Dsstox_cid_90
62. Aniline [hsdb]
63. Aniline [iarc]
64. Aniline [inci]
65. Aniline [mi]
66. Aniline [mart.]
67. Aniline [usp-rs]
68. Aniline [who-dd]
69. Chembl538
70. Epitope Id:117704
71. Ec 200-539-3
72. Aniline, Analytical Standard
73. Dsstox_rid_75359
74. Aniline, Ar, >=99%
75. Aniline, Lr, >=99%
76. Dsstox_gsid_20090
77. C6h5nh2
78. Discontinued, See H924510
79. Aniline [usp Impurity]
80. Dtxsid8020090
81. Bdbm92572
82. Trimethoprim Specified Impurity K
83. Aniline, Reagentplus(r), 99%
84. Benzene,amino (aniline)
85. Aniline [un1547] [poison]
86. Aniline 100 Microg/ml In Ethanol
87. Amy11081
88. Str00216
89. Aniline, Acs Reagent, >=99.5%
90. Tox21_200345
91. Aniline 10 Microg/ml In Cyclohexane
92. Stk301792
93. Zinc17886255
94. Akos000268796
95. Aniline 100 Microg/ml In Cyclohexane
96. Db06728
97. Aniline 1000 Microg/ml In Cyclohexane
98. Aniline, Astm, Acs Reagent, 99.5%
99. Aniline, Saj First Grade, >=99.0%
100. Cas-62-53-3
101. Aniline, Jis Special Grade, >=99.0%
102. Aniline, P.a., Acs Reagent, 99.0%
103. Ncgc00091297-01
104. Ncgc00091297-02
105. Ncgc00091297-03
106. Ncgc00257899-01
107. Bp-12047
108. Fentanyl Impurity F [ep Impurity]
109. Aniline, Pestanal(r), Analytical Standard
110. Db-013441
111. Mesalazine Impurity K [ep Impurity]
112. A0463
113. Ft-0622394
114. Ft-0662220
115. Ft-0696319
116. Trimethoprim Impurity K [ep Impurity]
117. C00292
118. A833829
119. Aminobenzoic Acid Impurity C [ep Impurity]
120. Q186414
121. Sr-01000944923
122. J-519591
123. Sr-01000944923-1
124. Q27121173
125. F2190-0417
126. Aniline, United States Pharmacopeia (usp) Reference Standard
127. 136260-71-4
| Molecular Weight | 93.13 g/mol |
|---|---|
| Molecular Formula | C6H7N |
| XLogP3 | 0.9 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 1 |
| Rotatable Bond Count | 0 |
| Exact Mass | 93.057849228 g/mol |
| Monoisotopic Mass | 93.057849228 g/mol |
| Topological Polar Surface Area | 26 Ų |
| 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 |
Carcinogens
Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included. (See all compounds classified as Carcinogens.)
/The objective was/ to study the permeability of intact mouse abdominal skin to aniline and the protective capability of two typical lab gloves against aniline. A Franz diffusion cell was used to perform in vitro transdermal absorption test and glove permeation test for aniline (0.102 mg/mL and 0.010 mg/mL). The permeabilities of intact mouse abdominal skin and gloves to aniline were measured by high performance liquid chromatography-diode array detection. The transdermal penetration of the two concentrations of aniline followed zero order kinetics within 12 hr, exhibiting total aniline permeabilities within 24 hr of 51.71% and 48.31%, respectively. The absorption liquid had an aniline concentration of at least 18 ug/L. The medical disposable latex glove could not stop the penetration of 0.010 mg/mL aniline, but the industrial natural latex glove could. The penetration of 0.102 mg/mL and 0.010 mg/mL aniline through the mouse abdominal skin follows zero order kinetics within 12 hr. The medical disposable latex glove cannot stop the penetration of 0.010 mg/mL aniline, but the industrial natural latex glove can.
PMID:23257095 Feng F et al; Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi 30 (9): 683-5 (2012)
The substance can be absorbed into the body by inhalation, through the skin also as a vapor and by ingestion.
International Program on Chemical Safety/European Commission; International Chemical Safety Card (ICSC) on Aniline (62-53-3) ICSC No. 0011 (April 2014). Available from, as of March 8, 2018: https://www.inchem.org/documents/icsc/icsc/eics0011.htm
(14)C-Aniline administered to rabbits is mostly excreted in urine (80% of dose) as conjugates of p-aminophenol (55%), o-aminophenol (10%), and m-aminophenol (0.1%), and as aniline (3.5%), aniline-N-glucuronide (6%), phenylsulfamic acid (8%), and acetanilide (0.2%). Only traces of the metabolites (1%) are excreted in feces, and no aniline is excreted in the expired air. ... Administration of high dose levels of aniline to rabbits results in the excretion of free glucuronic acid in the urine.
Parke, D. V. The Biochemistry of Foreign Compounds. Oxford: Pergamon Press, 1968., p. 224
Biliary excretion (% of dose excreted in 3 hr) of aniline in: rat 5.7%, guinea pig 5.6%, rabbit 2.6%, dog 2.7%, cat 0.3%, hen 1.6%. /From table; dose not given/
LaDu, B.N., H.G. Mandel, and E.L. Way. Fundamentals of Drug Metabolism and Disposition. Baltimore: Williams and Wilkins, 1971., p. 139
For more Absorption, Distribution and Excretion (Complete) data for Aniline (8 total), please visit the HSDB record page.
Aniline is an important source material in the chemical industry (e.g., rubber, pesticides, and pharmaceuticals). The general population is known to be ubiquitously exposed to aniline. Thus, assessment of aniline exposure is of both occupational and environmental relevance. Knowledge on human metabolism of aniline is scarce. We orally dosed four healthy male volunteers (two fast and two slow acetylators) with 5 mg isotope-labeled aniline, consecutively collected all urine samples over a period of 2 days, and investigated the renal excretion of aniline and its metabolites by LS-MS/MS and GC-MS. After enzymatic hydrolysis of glucuronide and sulfate conjugates, N-acetyl-4-aminophenol was the predominant urinary aniline metabolite representing 55.7-68.9% of the oral dose, followed by the mercapturic acid conjugate of N-acetyl-4-aminophenol accounting for 2.5-6.1%. Acetanilide and free aniline were found only in minor amounts accounting for 0.14-0.36% of the dose. Overall, these four biomarkers excreted in urine over 48 hr post-dose represented 62.4-72.1% of the oral aniline dose. Elimination half-times were 3.4-4.3 hr for N-acetyl-4-aminophenol, 4.1-5.5 hr for the mercapturic acid conjugate, and 1.3-1.6 and 0.6-1.2 hr for acetanilide and free aniline, respectively. Urinary maximum concentrations of N-acetyl-4-aminophenol were reached after about 4 hr and maximum concentrations of the mercapturic acid conjugate after about 6 hr, whereas concentrations of acetanilide and free aniline peaked after about 1 hr. The present study is one of the first to provide reliable urinary excretion factors for aniline and its metabolites in humans after oral dosage, including data on the predominant urinary metabolite N-acetyl-4-aminophenol, also known as an analgesic under the name paracetamol/acetaminophen.
PMID:26233686 Modick H et al; Arch Toxicol 90 (6): 1325-33 (2016)
In a 47-year-old woman ... acetanilide and acetaminophen were identified in plasma as metabolites of aniline.
PMID:10876991 Iwersen-Bergmann S, Schmoldt A; Int J legal Med 113 (3): 171-4 (2000)
Aniline is largely metabolized to conjugates of p-aminophenol, namely p-aminophenylglucuronide and p-acetamidophenylglucuronide.
Parke, D. V. The Biochemistry of Foreign Compounds. Oxford: Pergamon Press, 1968., p. 224
In addition to hydroxylation of aromatic ring, hydroxylation of amino group also occurs ... to give phenylhydroxylamine. Conjugation with cysteine also occurs and traces of o- and p-aminophenyl and p-acetamidophenyl-mercapturic acids have been detected in urine of rats and rabbits dosed with aniline.
Parke, D. V. The Biochemistry of Foreign Compounds. Oxford: Pergamon Press, 1968., p. 224
For more Metabolism/Metabolites (Complete) data for Aniline (14 total), please visit the HSDB record page.
Aniline has known human metabolites that include 4-aminophenol and N-Hydroxyaniline.
Aniline is a known human metabolite of Sudan I.
S73 | METXBIODB | Metabolite Reaction Database from BioTransformer | DOI:10.5281/zenodo.4056560
Whole body: 4 hours; [TDR, p. 100]
TDR - Ryan RP, Terry CE, Leffingwell SS (eds). Toxicology Desk Reference: The Toxic Exposure and Medical Monitoring Index, 5th Ed. Washington DC: Taylor & Francis, 1999., p. 100
Aniline exposure is associated with toxicity to the spleen leading to splenomegaly, hyperplasia, fibrosis and a variety of sarcomas of the spleen on chronic exposure. In earlier studies, we have shown that aniline exposure leads to iron overload, oxidative stress and activation of redox-sensitive transcription factors, which could regulate various genes leading to a tumorigenic response in the spleen. However, molecular mechanisms leading to aniline-induced cellular proliferation in the spleen remain largely unknown. This study was, therefore, undertaken on the regulation of G1 phase cell cycle proteins (cyclins), expression of cyclin-dependent kinases (CDKs), phosphorylation of retinoblastoma protein (pRB) and cell proliferation in the spleen, in an experimental condition preceding a tumorigenic response. Male SD rats were treated with aniline (0.5 mmol/kg/day via drinking water) for 30 days (controls received drinking water only), and splenocyte proliferation, protein expression of G1 phase cyclins, CDKs and pRB were measured. Aniline treatment resulted in significant increases in splenocyte proliferation, based on cell counts, cell proliferation markers including proliferating cell nuclear antigen (PCNA), nuclear Ki67 protein (Ki67) and minichromosome maintenance (MCM), MTT assay and flow cytometric analysis. Western blot analysis of splenocyte proteins from aniline-treated rats showed significantly increased expression of cyclins D1, D2, D3 and E, as compared to the controls. Similarly, real-time PCR analysis showed significantly increased mRNA expression for cyclins D1, D2, D3 and E in the spleens of aniline-treated rats. The overexpression of these cyclins was associated with increases in the expression of CDK4, CDK6, CDK2 as well as phosphorylation of pRB protein. Our data suggest that increased expression of cyclins, CDKs and phosphorylation of pRB protein could be critical in cell proliferation, and may contribute to aniline-induced tumorigenic response in the spleen.
PMID:21070798 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3076423 Wang J et al; Toxicol Appl Pharmacol 250 (2): 213-20 (2011)
Mechanisms by which aniline exposure elicits splenotoxicity, especially a tumorigenic response, are not well-understood. Earlier, we have shown that aniline exposure leads to oxidative DNA damage and up-regulation of OGG1 and NEIL1/2 DNA glycosylases in rat spleen. However, the contribution of endonuclease III homolog 1 (NTH1) and apurinic/apyrimidinic endonuclease 1 (APE1) in the repair of aniline-induced oxidative DNA damage in the spleen is not known. This study was, therefore, focused on examining whether NTH1 and APE1 contribute to the repair of oxidative DNA lesions in the spleen, in an experimental condition preceding tumorigenesis. To achieve this, male SD rats were subchronically exposed to aniline (0.5 mmol/kg/day via drinking water for 30 days), while controls received drinking water only. By quantitating the cleavage products, the activities of NTH1 and APE1 were assayed using substrates containing thymine glycol (Tg) and tetrahydrofuran, respectively. Aniline treatment led to significant increases in NTH1- and APE1-mediated BER activity in the nuclear extracts of spleen of aniline-treated rats compared to the controls. NTH1 and APE1 mRNA expression in the spleen showed 2.9- and 3.2-fold increases, respectively, in aniline-treated rats compared to the controls. Likewise, Western blot analysis showed that protein expression of NTH1 and APE1 in the nuclear extracts of spleen from aniline-treated rats was 1.9- and 2.7-fold higher than the controls, respectively. Immunohistochemistry indicated that aniline treatment also led to stronger immunoreactivity for both NTH1 and APE1 in the spleens, confined to the red pulp areas. These results, thus, show that aniline exposure is associated with induction of NTH1 and APE1 in the spleen. The increased repair activity of NTH1 and APE1 could be an important mechanism for the removal of oxidative DNA lesions. These findings thus identify a novel mechanism through which NTH1 and APE1 may regulate the repair of oxidative DNA damage in aniline-induced splenic toxicity.
PMID:23352893 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3725747 Ma H et al; Toxicol Appl Pharmacol 267 (3): 276-83 (2013)
The mechanisms by which aniline exposure elicits splenotoxic response, especially the tumorigenic response, are not well-understood. Earlier, we have shown that aniline-induced oxidative stress is associated with increased oxidative DNA damage in rat spleen. The base excision repair (BER) pathway is the major mechanism for the repair of oxidative DNA base lesions, and we have shown an up-regulation of 8-oxoguanine glycosylase 1 (OGG1), a specific DNA glycosylase involved in the removal of 8-hydroxy-2'-deoxyguanosine (8-OHdG) adducts, following aniline exposure. Nei-like DNA glycosylases (NEIL1/2) belong to a family of BER proteins that are distinct from other DNA glycosylases, including OGG1. However, contribution of NEIL1/2 in the repair of aniline-induced oxidative DNA damage in the spleen is not known. This study was, therefore, focused on evaluating if NEILs also contribute to the repair of oxidative DNA lesions in the spleen following aniline exposure. To achieve that, male SD rats were subchronically exposed to aniline (0.5 mmol/kg/day via drinking water for 30 days), while controls received drinking water only. The BER activity of NEIL1/2 was assayed using a bubble structure substrate containing 5-OHU (preferred substrates for NEIL1 and NEIL2) and by quantitating the cleavage products. Aniline treatment led to a 1.25-fold increase in the NEIL1/2-associated BER activity in the nuclear extracts of spleen compared to the controls. Real-time PCR analysis for NEIL1 and NEIL2 mRNA expression in the spleen revealed 2.7- and 3.9-fold increases, respectively, in aniline-treated rats compared to controls. Likewise, Western blot analysis showed that protein expression of NEIL1 and NEIL2 in the nuclear extract of spleens from aniline-treated rats was 2.0- and 3.8-fold higher than controls, respectively. Aniline treatment also led to stronger immunoreactivity for NEIL1 and NEIL2 in the spleens, confined to the red pulp areas. These studies, thus, show that aniline-induced oxidative stress is associated with an induction of NEIL1/2. The increased NIEL-mediated BER activity is another indication of aniline-induced oxidative damage in the spleen and could constitute another important mechanism of removal of oxidative DNA lesions, especially in transcribed DNA following aniline insult.
PMID:21145906 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3045817 Ma H et al; Toxicol Appl Pharmacol 25 1(1): 1-7 (2011)
/It is known/ that aniline exposure causes oxidative damage to the spleen. To further explore the oxidative mechanism of aniline toxicity, ... the potential contribution of heme oxygenase-1 (HO-1), which catalyzes heme degradation and releases free iron /was examined/. Male SD rats were given 1 mmol/kg/day aniline in water by gavage for 1, 4, or 7 days, and respective controls received water only. Aniline exposure led to significant increases in HO-1 mRNA expression in the spleen (2-and 2.4-fold at days 4 and 7, respectively) with corresponding increases in protein expression, as confirmed by ELISA and Western blot analysis. Furthermore, immunohistochemical assessment of spleen showed stronger immunostaining for HO-1 in the spleens of rats treated for 7 days, confined mainly to the red pulp areas. No changes were observed in mRNA and protein levels of HO-1 after 1 day exposure. The increase in HO-1 expression was associated with increases in total iron (2.4-and 2.7-fold), free iron (1.9-and 3.5-fold), and ferritin levels (1.9-and 2.1-fold) at 4 and 7 days of aniline exposure. Our data suggest that HO-1 up-regulation in aniline-induced splenic toxicity could be a contributing pro-oxidant mechanism, mediated through iron release, and leading to oxidative damage.
PMID:19969074 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2818702 Wang J et al; Free Radic Biol Med 48 (4): 513-8 (2010)
For more Mechanism of Action (Complete) data for Aniline (11 total), please visit the HSDB record page.
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