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1. Acid, Trichloroacetic
2. Acide Trichloracetique
3. Rubidium Trichloroacetate
4. Sodium Trichloroacetate
5. Trichloracetique, Acide
6. Trichloroacetate, Rubidium
7. Trichloroacetate, Sodium
1. 76-03-9
2. Acetic Acid, Trichloro-
3. Trichloroethanoic Acid
4. Aceto-caustin
5. Trichloracetic Acid
6. Trichloressigsaeure
7. Konesta
8. Acide Trichloracetique
9. Acido Tricloroacetico
10. Trichloroacetate
11. Amchem Grass Killer
12. 2,2,2-trichloroacetic Acid
13. Trichloorazijnzuur
14. Tca
15. Kyselina Trichloroctova
16. Acetic Acid, Trichloro- (solid)
17. Ccl3cooh
18. Trichloorazijnzuur [dutch]
19. Tkhu
20. Trichloressigsaeure [german]
21. Trichloroacetic Acid Solution
22. Tkhuk
23. Nsc 215204
24. Acide Trichloracetique [french]
25. Acido Tricloroacetico [italian]
26. Mfcd00004177
27. Nsc-215204
28. 5v2jdo056x
29. Chebi:30956
30. Acetic Acid, 2,2,2-trichloro-
31. Ncgc00091021-02
32. Wln: Qvxggg
33. Tecane
34. Trichloroacetic Acid Solid
35. Dsstox_cid_1378
36. Trichloorazijnzuur (dutch)
37. Dsstox_rid_76121
38. Dsstox_gsid_21378
39. Trichloressigsaeure (german)
40. Acide Trichloracetique (french)
41. Acido Tricloroacetico (italian)
42. Caswell No. 870
43. Sodiumtrichloroacetate
44. Cas-76-03-9
45. Smr000059159
46. Trichloroacetic Acid (iupac)
47. Trichloromethanecarboxylic Acid
48. Tcaa
49. Trichloro Acetic Acid
50. Ccris 4015
51. Kyselina Trichloroctova [czech]
52. Hsdb 1779
53. Einecs 200-927-2
54. Un1839
55. Un2564
56. Tca [bsi:iso]
57. Epa Pesticide Chemical Code 081002
58. Trichloroacetic Acid [usp]
59. Brn 0970119
60. Unii-5v2jdo056x
61. Ai3-24157
62. Trichloressigsaure
63. Tricloroacetic Acid
64. Perchloroacetic Acid
65. Trichloroacetic-acid
66. Trichloro-acetic Acid
67. Varitox (salt/mix)
68. Ccl3co2h
69. Na Ta (salt/mix)
70. Tca [iso]
71. Ec 200-927-2
72. Acido Tricloroacetico (tn)
73. Schembl3220
74. Nciopen2_000772
75. 4-02-00-00508 (beilstein Handbook Reference)
76. Mls001066365
77. Mls001336033
78. Mls001336034
79. Un 2564 (salt/mix)
80. Chembl14053
81. Trichloroacetic Acid, Solution
82. Trichloroacetic Acid-[2-13c]
83. Dtxsid1021378
84. Trichloroacetic Acid [mi]
85. Trichloroacetic Acid Solid (dot)
86. Trichloroacetic Acid, >=99.5%
87. Trichloroacetic Acid, Acs Reagent
88. Hms2233m06
89. Hms3374m09
90. Trichloroacetic Acid [hsdb]
91. Nsc77363
92. Str02719
93. Zinc3791092
94. Tox21_111060
95. Tox21_201632
96. Tox21_300187
97. Trichloroacetic Acid [vandf]
98. Trichloroacetic Acid Solution (dot)
99. Nsc-77363
100. Nsc215204
101. Stl163550
102. Trichloroacetic Acid [mart.]
103. Trichloroacetic Acid [who-dd]
104. Akos000118939
105. Trichloroacetic Acid (acd/name 4.0)
106. Trichloroacetic Acid Solution, 0.6 N
107. Trichloroacetic Acid Solution, 6.1 N
108. Un 1839
109. Ncgc00091021-01
110. Ncgc00091021-03
111. Ncgc00091021-04
112. Ncgc00254060-01
113. Ncgc00259181-01
114. Nci60_006100
115. Trichloroacetic Acid [ep Impurity]
116. Trichloroacetic Acid, Reagent Grade, 98%
117. Trichloroacetic Acid [ep Monograph]
118. Trichloroacetic Acid, Bioxtra, >=99.0%
119. Ft-0645145
120. T0369
121. Trichloroacetic Acid, >=99.0% (titration)
122. Trichloroacetic Acid [un1839] [corrosive]
123. Trichloroacetic Acid, 5% W/v Aqueous Solution
124. Trichloroacetic Acid, Acs Reagent, >=99.0%
125. D08633
126. E78851
127. Trichloroacetic Acid, 10% W/v Aqueous Solution
128. Tca Deblock, 3 % (w/v) In Methylene Chloride
129. Trichloroacetic Acid, Bioultra, >=99.5% (t)
130. Q410116
131. Trichloroacetic Acid, Purum P.a., >=99.0% (t)
132. J-525058
133. Trichloroacetic Acid, Jis Special Grade, >=99.0%
134. F1908-0096
135. Trichloroacetic Acid, Pestanal(r), Analytical Standard
136. Trichloroacetic Acid, Solution [un2564] [corrosive]
137. Z1270446580
138. Trichloroacetic Acid Solution, ~6.25 % (w/v), 0.38 N
139. Trichloroacetic Acid Solution, 6.1 N (approx. 100% W/v)
140. Trichloroacetic Acid, Biotech. Grade, Redistilled, >=99%
141. Trichloroacetic Acid, Puriss. P.a., Acs Reagent, >=99.5%
142. Deblock Trichloroacetic Acid Solution, 3% W/w In Dichloromethane
143. Deblock Trichloroacetic Acid Solution, 3 % (w/v) In Methylene Chloride
144. Trichloroacetic Acid Solution, Certified Reference Material, 1000 Mug/ml In Methyl Tert-butyl Ether
145. Trichloroacetic Acid, Acs Reagent, For The Determination Of Fe In Blood According To Heilmeyer, >=99.5%
146. Trichloroacetic Acid, For Electrophoresis, Suitable For Fixing Solution (for Ief And Page Gels), >=99%
147. Trichloroacetic Acid, Puriss., Meets Analytical Specification Of Ph. Eur., Usp 21, 99-100.5% (calc. To The Dried Substance)
| Molecular Weight | 163.38 g/mol |
|---|---|
| Molecular Formula | C2HCl3O2 |
| XLogP3 | 1.3 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 2 |
| Rotatable Bond Count | 0 |
| Exact Mass | 161.904212 g/mol |
| Monoisotopic Mass | 161.904212 g/mol |
| Topological Polar Surface Area | 37.3 Ų |
| Heavy Atom Count | 7 |
| Formal Charge | 0 |
| Complexity | 83.4 |
| 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 |
Caustics
National Library of Medicine's Medical Subject Headings online file (MeSH, 2007)
Epithelial implantation cysts of anterior chamber /eye/ have been treated in human ... by injection of 10% trichloroacetic acid ... .
Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 933
Clinically ... has been used in 10% to 25% aq soln to cauterize surface of cornea in treatment of recurrent erosion, bullous keratopathy, & other painful corneal diseases.
Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 933
The use of trichloracetic acid in the treatment of decorative tattoos is described. The technique is simple to perform. No anesthesia or analgesia is required. Complications are uncommon and usually minor. Trichloracetic acids acts by inflicting burn.
PMID:2251635 Hudson DA, Lechtape-Gruter RU; S Afr Med J 78 (12): 748-749 (1990)
For more Therapeutic Uses (Complete) data for TRICHLOROACETIC ACID (12 total), please visit the HSDB record page.
47-year-old woman presented with a history of yellow plaques on her eyelids. These lesions had been diagnosed clinically as xanthelasma and treated five times with topical applications of trichloroacetic acid (TCA) 33 percent. Despite flattening of the original lesions, the patient noticed extension of the lesions on the site of treatment following each session. Skin biopsy showed characteristic findings of xanthelasma. It appears that, in rare instances, xanthelasma palpebrarum may progress following TCA application by a Koebner-like phenomenon.
PMID:16638405 Akhyani M et al; Dermatol Online J 12 (2): 12 (2006)
...Trichloroacetic acid is not significantly absorbed and therefore does not produce systemic complications /from use for chemexfoliation (chemical peeling). Both phenol and trichloroacetic acid may produce hypertrophic scars and/or keloids and pigmentation irregularities, may accentuate preexisting abnormalities (eg, telangiectasias, nevi, and pores), and may be associated with a flare of latent herpes virus infection. Prolonged erythema of the treated areas and persistent rhytides have been reported with both agents.
PMID:3611440 Lober CW; J Am Acad Dermatol 17 (1): 109-12 (1987)
A 32-year-old healthy female was examined one day after undergoing a face-peeling procedure with a mask containing trichloroacetic acid. She complained of severe burning, redness, and epiphora in her left eye that started several hours after the procedure. Her vision was LE 0.2, RE 0.8. Mild upper eyelid edema of the right eye and severe edema of the left eyelids, LE inferior ectropion, and LE blepharoconjunctivitis were noted. The conjunctiva was severely hyperemic with papillary reaction and chemosis. The corneas, anterior chambers, irides, lenses, and posterior segments were normal. The patient was treated with Dexamethasone 0.1% q2h and ocular lubrication. The reaction subsided after 3-4 days.
PMID:16019688 Kaiserman I and Kaiserman N; Ocul Immunol Inflamm 13 (2-3): 257-9 (2005)
Caustics
Strong alkaline chemicals that destroy soft body tissues resulting in a deep, penetrating type of burn, in contrast to corrosives, that result in a more superficial type of damage via chemical means or inflammation. Caustics are usually hydroxides of light metals. SODIUM HYDROXIDE and potassium hydroxide are the most widely used caustic agents in industry. Medically, they have been used externally to remove diseased or dead tissues and destroy warts and small tumors. The accidental ingestion of products (household and industrial) containing caustic ingredients results in thousands of injuries per year. (See all compounds classified as Caustics.)
After trichloroethylene poisoning, TCA is excreted in urine in high quantities that quickly decr but are detectable for some time. Excretion pattern of TCA in perchloroethylene poisoning is quite variable.
WEISS G; ZENTR ARBEITSMED ARBEITSCHUTZ 19 (5): 143-6 (1969)
TCA is ... not readily absorbed through the skin.
American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1603
After trichloroethylene absorption trichloroacetic acid occurs as an intermed that is excreted in the urine as glucuronic acid. /From table/
Browning, E. Toxicity and Metabolism of Industrial Solvents. New York: American Elsevier, 1965., p. 192
Administration of a single oral dose of 5, 20, or 100 mg/kg (14)C-TCA to male F344 rats or male B6C3F1 mice was followed by elimination of >50% of the dose as the parent compound in urine. Initial circulating concentrations of the parent TCA were 40% higher in rats (reflected in significantly larger plasma AUC values) than in mice; twice the percentage of TCA was exhaled as (14)CO2 compared to that in mice. After the first 3 hours, elimination kinetics for the two species were essentially identical (plasma t1/2= 5.8 hours).
American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1603
... Absorption and distribution studies were conducted with radiolabelled trichloro(2-(14)C)acetic acid, which was administered by gavage (500 mg/kg) as aqueous free acid, neutral aqueous solution (sodium salt) or free acid in corn oil. The absorption and distribution of trichloroacetic acid was similar in all cases: the chemical was absorbed rapidly after dosing, maximum plasma liver concn of free radiolabel being achieved in <1 hr. ...
Styles JA et al; Carcinogenesis (Eynsham) 12 (9): 1715-20 (1991)
TCA is a metabolite of chloral hydrate.
PMID:5451363 CABANA BE, GESSNER PK; J PHARMACOL EXP THER 174 (2): 260-75 (1970)
A group of 10 men and 10 women employed for the production of polyethylene bags, for which trichloroethylene is used, were examined. The analysis of TCA content in urine shows a 40% reduction after 2 days rest.
Soleo L et al; Riv Med Lav Ig Ind 3 (April-June): 127-42 (1979)
Interaction of tetrachloroethylene with hepatic microsomal cytochromes p450 was investigated using male Long-Evans rats. Free trichloroacetic acid was the major metabolite of tetrachloroethylene from the hepatic microsomal cytochrome p450 system.
PMID:7437086 Costa AK, Ivanetich KM; Biochem Pharmacol 29 (20): 2863-70 (1980)
After exposure of workers to trichloroethylene, urinary concentration of trichloroacetic acid was related to trichloroethylene vapor concentration up to 50 ppm, but not at higher concentrations.
PMID:5044605 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1009432 Ikeda M et al; Br J Ind Med 29 (3): 328-33 (1972)
For more Metabolism/Metabolites (Complete) data for TRICHLOROACETIC ACID (11 total), please visit the HSDB record page.
After administration of a single oral dose of 3 mg/kg bw trichloroacetic acid to healthy volunteers, the mean plasma half life of the compound was about 50 hr and the volume of distribution was about 115 mL/kg bw.
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. V63 300 (1995)
Trichloroethylene may act as a promoter, because it inhibits intercellular communication in vitro. It is converted to trichloroacetic acid (TCA) in mice, but not much in rats. TCA acts as a peroxisome proliferator, and the neoplasm in the liver of mice may arise through this mechanism. These chemicals are conjugated with GSH, yielding products that are converted to the reactive metabolites in the kidneys through the action of beta-lyase. These steps occur to a greater extent in rats than in mice, and account for the pronounced nephrotoxicity, involving alpha-2-microglobin accumulation, probably a key reaction. The nephrotoxicity explains the low but definite yield of kidney neoplasms.
Amdur, M.O., J. Doull, C.D. Klaasen (eds). Casarett and Doull's Toxicology. 4th ed. New York, NY: Pergamon Press, 1991., p. 193
Induction of peroxisome proliferation has been repeatedly associated with the chronic toxicity and carcinogenicity of trichloroacetic acid to the liver ... It can induce peroxisome proliferation in the livers of both mice and rats, as indicated by increased activities of palmitoyl-coenzyme A oxidase and carnitine acetyl transferase, the appearance of peroxisome proliferation associated protein and increased volume density of peroxisomes after exposure to trichloroacetic acid for 14 days. The compound induced peroxisome proliferation in mouse but not in rat kidney, and it induced peroxisome proliferation in primary cultures of hepatocytes from rats and mice but not in those from humans.
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. V63 302 (1995)
A linear dose response relation /was found/ between TCA induced hepatocellular nodules and proliferative lesions in male mice given the compound in their drinking water at 1000 to 2000 ppm for 1 year. Hepatocellular hypertrophy with intracellular glycogen and a marked accumulation of lipofuscin (indicative of massive intracellular lipid peroxidation) developed. These data suggest that TCA induced hepatotoxicity in mice was related to the generation of free radicals during its in vivo biotransformation. Neither necrosis nor hyperplasia were seen in TCA exposed mice.
American Conference of Governmental Industrial Hygienists, Inc. Documentation of the Threshold Limit Values and Biological Exposure Indices. 6th ed. Volumes I, II, III. Cincinnati, OH: ACGIH, 1991., p. 1602
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