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1. Ethinyl Trichloride
2. Trichloride, Ethinyl
3. Trichloroethene
4. Trielina
5. Trilene
1. Trichloroethene
2. 79-01-6
3. 1,1,2-trichloroethene
4. Ethene, Trichloro-
5. Ethylene Trichloride
6. Ethinyl Trichloride
7. 1,1,2-trichloroethylene
8. Acetylene Trichloride
9. Anamenth
10. Densinfluat
11. Germalgene
12. Narcogen
13. Narkosoid
14. Westrosol
15. Trilene
16. Trichlorethylene
17. Chlorilen
18. Trethylene
19. Trielina
20. Triciene
21. Blancosolv
22. Crawhaspol
23. Threthylen
24. Threthylene
25. Trichloraethen
26. Trichloran
27. Trichloren
28. Algylen
29. Benzinol
30. Blacosolv
31. Cecolene
32. Chlorylen
33. Circosolv
34. Dukeron
35. Lanadin
36. Lethurin
37. Petzinol
38. Triasol
39. Trielene
40. Trielin
41. Trieline
42. Vestrol
43. Fluate
44. Nialk
45. Philex
46. Trial
47. Trilen
48. Trimar
49. Vitran
50. Fleck-flip
51. Flock Flip
52. Tri-plus
53. Triklone N
54. Dow-tri
55. Tri-clene
56. Perm-a-chlor
57. 1,1-dichloro-2-chloroethylene
58. 1-chloro-2,2-dichloroethylene
59. Tri-plus M
60. Trichlooretheen
61. Tricloretene
62. Tricloroetilene
63. Trichlorethylenum
64. Trichloroethylenum
65. Trichloraethylenum
66. 1,2,2-trichloroethylene
67. Tricloroetileno
68. Chlorylea
69. Chorylen
70. Ethylene, Trichloro-
71. Gemalgene
72. Narkogen
73. Trichloraethylen, Tri
74. Trichlorethylene, Tri
75. Triklone
76. Triline
77. Triol
78. Trichloorethyleen, Tri
79. Trilene Te-141
80. Ethene, 1,1,2-trichloro-
81. Tricloroetilene [dcit]
82. Tce (chlorohydrocarbon)
83. C2hcl3
84. Trichloroethylene [inn]
85. Perm-a-clor
86. Rcra Waste Number U228
87. Trichloroethylene (iupac)
88. Trichlor
89. Trichlorethene
90. Trichloraethylen
91. Nci-c04546
92. Distillex Ds2
93. R 1120
94. Un 1710
95. Tri
96. Trichloroethylene (without Epichlorohydrin)
97. Trichloraethylenum Pro Narcosi
98. Chebi:16602
99. 290ye8ar51
100. Ncgc00091202-01
101. Dsstox_cid_1382
102. Dsstox_rid_76125
103. Dsstox_gsid_21383
104. 123919-09-5
105. Trielina [italian]
106. Caswell No. 876
107. Trichlorathane
108. Tricloretene [italian]
109. Triclene
110. Densi Nfluat
111. Trichlooretheen [dutch]
112. Trichloraethen [german]
113. Trichloroethylene (tce)
114. Trik Lone
115. Tric Hloroethene
116. Mfcd00000838
117. Tricloroetilene [italian]
118. Trichloro Ethylene
119. .beta.-d-ribo-hexopyranose, 1,6-anhydro-3-deoxy-2-o-methyl-4-o-(2-methylpentyl)-
120. Cas-79-01-6
121. Ccris 603
122. Trichloroethene 100 Microg/ml In Methanol
123. Trichloride, Ethinyl
124. Trichloroethene 1000 Microg/ml In Methanol
125. Trichloroethylene, Acs Reagent, >=99.5%
126. Tricloroetileno [inn-spanish]
127. Hsdb 133
128. Trichloorethyleen, Tri [dutch]
129. Trichloraethylen, Tri [german]
130. Trichlorethylene, Tri [french]
131. Trichloroethylenum [inn-latin]
132. Nsc 389
133. Einecs 201-167-4
134. Un1710
135. Rcra Waste No. U228
136. Epa Pesticide Chemical Code 081202
137. Brn 1736782
138. Trichloroethylene [inn:nf]
139. Trichlorothene
140. Unii-290ye8ar51
141. Trichloro-ethene
142. Ai3-00052
143. Disparit B
144. Trichloro-ethylene
145. Altene Dg
146. F 1120
147. Trichloroethene, 9ci
148. Trichloroethylene [un1710] [poison]
149. Trichloroethylene (with Epichlorohydrin)
150. 1,1,1-trichloroethylene
151. 1,1,2-trichloro-ethene
152. Ec 201-167-4
153. Trichloroethylene, Anhydrous
154. Schembl5754
155. Trichloroethylene, >=99%
156. Trichloroethylene, Stabilized
157. 4-01-00-00712 (beilstein Handbook Reference)
158. Chlorylea, Chorylen, Circosolv, Crawhaspol, Dow-tri, Dukeron, Per-a-clor, Triad, Trial, Tri-plus M, Vitran
159. Trichloroethylene [ii]
160. Trichloroethylene [mi]
161. 1,1,2-tris(chloranyl)ethene
162. Trichloroethylene [fcc]
163. Chembl279816
164. Trichloroethylene [hsdb]
165. Trichloroethylene [iarc]
166. Dtxsid0021383
167. Trichloroethylene, P.a., 98%
168. Trichloroethylene, Lr, >=99%
169. Trichloroethylene [mart.]
170. Trichloroethylene [usp-rs]
171. Trichloroethylene [who-dd]
172. Trichloroethylene, Electronic Grade
173. Trichloroethylene Reagent Grade Acs
174. Zinc8214699
175. Tox21_111101
176. Tox21_202543
177. Stl282732
178. Trichloroethylene, Analytical Standard
179. Trichloroethylene, Semiconductor Grade
180. Akos000118838
181. Ccg-230934
182. Db13323
183. Ncgc00091202-02
184. Ncgc00091202-03
185. Ncgc00260092-01
186. Trichloroethylene [un1710] [poison]
187. Trichloroethene 10 Microg/ml In Methanol
188. Trichloroethylene, Spectrophotometric Grade
189. C06790
190. Trichloroethylene, Saj First Grade, >=98.0%
191. Trichloroethylene, Jis Special Grade, >=99.5%
192. A839551
193. Q407936
194. J-504494
195. Trichloroethylene, Puriss. P.a., >=99.5% (gc)
196. Brd-k46435528-001-01-0
197. Trichloroethylene, Spectrophotometric Grade, >=99.5%
198. F0001-2068
199. Trichloroethylene, Anhydrous, Contains 40 Ppm Diisopropylamine As Stabilizer, >=99%
200. Trichloroethylene, Pharmaceutical Secondary Standard; Certified Reference Material
201. Trichloroethylene, Reagent Grade, >=99.0%, Contains ~1% 1,2-epoxybutane As Inhibitor
202. Residual Solvent - Trichloroethylene, Pharmaceutical Secondary Standard; Certified Reference Material
203. Tcv
| Molecular Weight | 131.38 g/mol |
|---|---|
| Molecular Formula | C2HCl3 |
| XLogP3 | 2.6 |
| Hydrogen Bond Donor Count | 0 |
| Hydrogen Bond Acceptor Count | 0 |
| Rotatable Bond Count | 0 |
| Exact Mass | 129.914383 g/mol |
| Monoisotopic Mass | 129.914383 g/mol |
| Topological Polar Surface Area | 0 Ų |
| Heavy Atom Count | 5 |
| Formal Charge | 0 |
| Complexity | 42.9 |
| 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 |
Anesthetics, Inhalation; Solvents
National Library of Medicine's Medical Subject Headings. Trichloroethylene. Online file (MeSH, 2016). Available from, as of December 2, 2016: https://www.nlm.nih.gov/mesh/2016/mesh_browser/MBrowser.html
/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Trichloroethylene is included in the database.
NIH/NLM; ClinicalTrials.Gov. Available from, as of February 1, 2017: https://clinicaltrials.gov/ct2/results?term=Trichloroethylene+&Search=Search
Medication (Vet): Anestheic (inhalation) /Former use/
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1786
Dental anesthetic. /Former use in USA/
WHO; Environ Health Criteria 50: Trichloroethylene p.31 (1985)
Anesthetic (inhalation) /Former use/
O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 1786
Patients exposed to trichloroethylene should be warned of the potential adverse effects of ethanol ingestion.
Hansten, P.D. Drug Interactions. 4th ed. Philadelphia: Lea and Febiger, 1979., p. 219
...Its anesthetic action is weak. Its low volatility appears in part to be responsible for this effect. ... Apparatus that employs bubbling oxygen assists in accelerating the volatility of the anesthetic to increase its potency. Because of its inherent weakness as an anesthetic, induction of anesthesia is slow. Cardiac arrhythmias produced by the anesthetic are unfavorable. Trichloroethylene cannot be used in a closed circuit with soda lime because of formation of a toxic product.
Booth, N.H., L.E. McDonald (eds.). Veterinary Pharmacology and Therapeutics. 5th ed. Ames, Iowa: Iowa State University Press, 1982., p. 195
Relaxation of abdominal musculature is poor during trichloroethylene anesthesia.This effect is similar to other agents (eg, ketamine, alpha-chloralose) that do not induce Stage III anesthesia. Trichloroethylene is considered unsatisfactory for this type of surgery unless it is used in conjunction with a skeletal muscle relaxant. It has very little if any effect upon uterine function. It readly crosses the placenta to reach the fetal circulation of sheep, goats, and probably other species.
Booth, N.H., L.E. McDonald (eds.). Veterinary Pharmacology and Therapeutics. 5th ed. Ames, Iowa: Iowa State University Press, 1982., p. 195
... The estimated fatal oral dose in humans is 3-5 mL/kg. The lowest concentration produce unconsciousness in adult humans is 16 mg/L (3,000 ppm); the equivalent oral dose is 40-150 mL.
Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-165
Solvents
Liquids that dissolve other substances (solutes), generally solids, without any change in chemical composition, as, water containing sugar. (Grant and Hackh's Chemical Dictionary, 5th ed) (See all compounds classified as Solvents.)
Anesthetics, Inhalation
Gases or volatile liquids that vary in the rate at which they induce anesthesia; potency; the degree of circulation, respiratory, or neuromuscular depression they produce; and analgesic effects. Inhalation anesthetics have advantages over intravenous agents in that the depth of anesthesia can be changed rapidly by altering the inhaled concentration. Because of their rapid elimination, any postoperative respiratory depression is of relatively short duration. (From AMA Drug Evaluations Annual, 1994, p173) (See all compounds classified as Anesthetics, Inhalation.)
N - Nervous system
N01 - Anesthetics
N01A - Anesthetics, general
N01AB - Halogenated hydrocarbons
N01AB05 - Trichloroethylene
Blood and urine samples were collected in 1990 from 10 people working in four dry cleaning shops in Croatia, where trichloroethylene was used as the cleaning solvent. The concentration of trichloroethylene in the air was 25-40 ppm [134-215 mg/cu m]. The mean blood levels of trichloroethylene were 0.38 umol/L [50 ug/L] on Monday morning (range, 0.15- 3.58 umol/L) (20-70 ug/L) and 3.39 umol/L [445 ug/L] on Wednesday afternoon (range, 0.46- 12.71 umol/L (60-1670 ug/L]. ...
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 90 1995
TCE is rapidly absorbed into the systemic circulation via the oral and inhalation routes. The majority of TCE undergoes oxidation in the liver by CYPs, with a small proportion being conjugated with glutathione (GSH) via glutathione S-transferases (GSTs). Thus, two distinct metabolic pathways exist for TCE. ... TCE may be oxidized to yield one of three initial metabolites: chloral, TCE-epoxide, and dichloroacetylchloride. These metabolites rapidly undergo oxidation and/or reduction to yield trichloroacetate (TCA) and trichloroethanol (TCOH), the major end products of the oxidative pathway. TCOH is either oxidized to TCA or glucuronidated. TCOH glucuronide is excreted via the urine and bile. That in the bile may undergo enterohepatic recirculation by hydrolysis to TCOH in the gut, with reabsorption and the possibility of conversion to TCA. TCA accumulates in the body due to strong plasma protein binding and slow excretion. In contrast, blood levels of DCA, formed by TCA dechlorination or from TCOH, are very low or nondetectable in humans. Relatively small amounts of TCE can be conjugated in the liver with GSH to form S-(1,2-dichlorovinyl)glutathione (DCVG). DCVG is then effluxed from the hepatocyte into plasma and bile for translocation to the kidney and small intestine, respectively. The plasma DCVG is intrarenally converted by gamma-glutamyltransferase and dipeptidases to the cysteine conjugate S-(1,2-dichlorovinyl)-L-cysteine (DCVC). The DCVG secreted into the bile can undergo extrarenal processing to DCVC, that is subsequently delivered to the kidney by enterohepatic recirculation. DCVC represents a branch point in the pathway. It may be detoxified through N-acetylation or bioactivated to reactive thiols via renal beta-lyase located in renal proximal tubular cells (or to a lesser extent, bioactivated to DCVC sulfoxide via flavin-containing monooxygenases).
Klaassen, C.D. (ed). Casarett and Doull's Toxicology. The Basic Science of Poisons. 7th ed. New York, NY: McGraw-Hill, 2008., p. 998
TCE is rapidly and extensively absorbed by all routes of environmental exposure, including oral ingestion, inhalation and skin contact. Absorbed TCE is distributed throughout the body, where it can accumulate in fat and other tissues.
American Conference of Governmental Industrial Hygienists. Documentation of the TLVs and BEIs with Other World Wide Occupational Exposure Values. 7th Ed. CD-ROM Cincinnati, OH 45240-1634 2013., p. 5
... The pharmacokinetics of trichloroethylene (TCE) in male Sprague-Dawley (S-D) rats were characterized (1) during and after inhalation exposure to 50 or 500 ppm TCE, (2) following administration of 8 mg/kg TCE PO, and (3) following intra-arterial injection of 8 mg/kg TCE. Blood and tissues (including liver, kidney, fat, skeletal muscle, heart, spleen, gastrointestinal tract, and brain) were collected at selected time-points from 5 min up to 24 hr post initial exposure. The fat compartment was modified to be diffusion-limited to predict the observed slow release of TCE from the fat. The addition of a deep liver compartment was necessary to accurately predict the slower hepatic clearance of TCE for all three exposure routes. Simulations of liver concentrations following gavage of male B6C3F1 mice with 300-2000 mg/kg TCE were also improved with the addition of a deep liver compartment. Liver predictions were calibrated and validated using a cross-validation technique novel to PBPK modeling. Splitting of compartments did not significantly affect predictions of TCE concentrations in the liver, fat, or venous blood. ...
PMID:12915716 Keys DA et al; Toxicol Sci 76 (1): 35-50 (2003)
For more Absorption, Distribution and Excretion (Complete) data for Trichloroethylene (23 total), please visit the HSDB record page.
... We collected urine from Hartley male and female guinea pigs 24 hours after intracutaneous injection of trichloroethylene (TRI), trichloroethanol (TCE) or trichloroacetic acid (TCA) during a guinea pig maximization test and measured the urinary metabolites by gas chromatography-mass spectrometry. After TRI treatment, the amount of TCA was significantly greater in females than males, while there was no sex difference in the total amount (TCA + TCE). TCA was only detected in urine after TCA treatment. Interestingly, not only TCE but also TCA was detected in urine of both sexes after TCE treatment, and the amount of TCA was also greater in females than males. An additional experiment showed that TCE treatment did not result in the detection of urinary TCA in cytochrome P450 (CYP)2E1-null mice TCE but did in wild-type mice, suggesting the involvement of CYP2E1 in the metabolism from TCE to TCA. The constitutive expression of CYP2E1 in the liver of guinea pigs was greater in females than males. The sex difference in urinary TCA excretion after TRI and TCE treatments may be due to variation of the constitutive expression of CYP2E1.
PMID:24025858 Hibino Y et al; J Occup Health 55 (6): 443-9 (2013)
Toxicological interactions with drugs have the potential to modulate the toxicity of trichloroethylene (TCE). Our objective is to identify metabolic interactions between TCE and 14 widely used drugs in human suspended hepatocytes and characterize the strongest using microsomal assays. Changes in concentrations of TCE and its metabolites were measured by headspace GC-MS. Results with hepatocytes show that amoxicillin, cimetidine, ibuprofen, mefenamic acid and ranitidine caused no significant interactions. Naproxen and salicylic acid showed to increase both TCE metabolites levels, whereas acetaminophen, carbamazepine and erythromycin rather decreased them. Finally, diclofenac, gliclazide, sulphasalazine and valproic acid had an impact on the levels of only one metabolite. Among the 14 tested drugs, 5 presented the most potent interactions and were selected for confirmation with microsomes, namely naproxen, salicylic acid, acetaminophen, carbamazepine and valproic acid. Characterization in human microsomes confirmed interaction with naproxen by competitively inhibiting trichloroethanol (TCOH) glucuronidation (Ki=2.329 mM). Inhibition of TCOH formation was also confirmed for carbamazepine (partial non-competitive with Ki=70 uM). Interactions with human microsomes were not observed with salicylic acid and acetaminophen, similar to prior results in rat material. For valproic acid, interactions with microsomes were observed in rat but not in human. Inhibition patterns were shown to be similar in human and rat hepatocytes, but some differences in mechanisms were noted in microsomal material between species. ...
PMID:24632077 Cheikh Rouhou M, Haddad S; Toxicol In Vitro 28 (5): 732-41 (2014)
... In this study we have compared the renal toxicity of TCE and /its major metabolite trichloroethanol/ (TCE-OH) in rats to try and ascertain whether the glutathione pathway or formic aciduria can account for the toxicity. Male rats were given TCE (500 mg/kg/day) or TCE-OH at (100 mg/kg/day) /by oral gavage/ for 12 weeks and the extent of renal injury measured at several time points using biomarkers of nephrotoxicity and prior to termination assessing renal tubule cell proliferation. The extent of formic aciduria was also determined at several time points, while renal pathology and plasma urea and creatinine were determined at the end of the study. TCE produced a very mild increase in biomarkers of renal injury, total protein, and glucose over the first two weeks of exposure and increased Kim-1 and NAG in urine after 1 and 5 weeks exposure, while TCE-OH did not produce a consistent increase in these biomarkers in urine. However, both chemicals produced a marked and sustained increase in the excretion of formic acid in urine to a very similar extent. The activity of methionine synthase in the liver of TCE and TCE-OH treated rats was inhibited by about 50% indicative of a block in folate synthesis. Both renal pathology and renal tubule cell proliferation were reduced after TCE and TCE-OH treatment compared to controls. Our findings do not clearly identify the pathway which is responsible for the renal toxicity of TCE but do provide some support for metabolism via glutathione conjugation.
PMID:24923549 Yaqoob N et al; Toxicology 323: 70-7 (2014)
Extraplacental membranes define the gestational compartment and provide a barrier to infectious microorganisms ascending the gravid female reproductive tract. We tested the hypothesis that bioactive metabolites of trichloroethylene (TCE) decrease pathogen-stimulated innate immune response of extraplacental membranes. Extraplacental membranes were cultured for 4, 8, and 24 hr with the TCE metabolites trichloroacetate (TCA) or S-(1,2-dichlorovinyl)-l-cysteine (DCVC) in the absence or presence of lipoteichoic acid (LTA) or lipopolysaccharide (LPS) to simulate infection. In addition, membranes were cocultured with DCVC and Group B Streptococcus (GBS). DCVC (5-50 uM) significantly inhibited LTA-, LPS-, and GBS-stimulated cytokine release from tissue cultures as early as 4 hr (P
PMID:25653212 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4426062 Boldenow E et al; Reprod Toxicol 52: 1-6 (2015)
For more Metabolism/Metabolites (Complete) data for Trichloroethylene (24 total), please visit the HSDB record page.
Trichloroethylene has known human metabolites that include Chloral hydrate.
S73 | METXBIODB | Metabolite Reaction Database from BioTransformer | DOI:10.5281/zenodo.4056560
Whole body: 53 hours; for trichloroethanol in blood: 12 hours; for trichloroacetic acid in urine: 75 hours; [TDR, p. 1181]
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. 1181
The biological half-lives of the urinary metabolites of humans occupationally exposed to trichloroethylene /is/ approx 41 hours.
Ikeda M, Imamura T; Int Arch Arbeitsmed 31 (3): 209-24 (1973)
The half-life of trichloroethylene in exhaled air & in the blood depends on the length of exposure & on the time of sampling after exposure. ... Maximum concentration /of trichloroethanol/ in blood & urine /is reached/ almost directly after exposure. ... concentration decreases with a half-life of about 10-15 hr. ... Concentration of trichloroacetic acid in both the blood & urine increases for up to 20-40 hr after /a single/ exposure. ... concentration decreases with a half-life of about 70-100 hr.
WHO; Environ Health Criteria 50: Trichloroethylene p.48 (1985)
Trichloroethanol and its glucuronide are rapidly eliminated in urine, with half-lives of about 10 hr, and trichloroacetic acid is eliminated slowly, with a half-life of about 52 hr (range, 35-70 hr).
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 112 (1995)
... Trichloroethylene has an estimated half- life in humans in venous blood of 21.7 hours ... .
National Research Council; Committee on Human Health Risks of Trichloroethylene; Assessing the Human Health Risks of Trichloroethylene: Key Scientific Issues p. 185 (2006). Available from, as of December 1, 2016: https://www.nap.edu/catalog/11707.html
For more Biological Half-Life (Complete) data for Trichloroethylene (8 total), please visit the HSDB record page.
Trichloroethylene (TCE), dichloroacetic acid (DCA), and trichloroacetic acid (TCA) are environmental contaminants that are carcinogenic in mouse liver. 5-Methylcytosine (5-MeC) in DNA is a mechanism that controls the transcription of mRNA, including the protooncogenes, c-jun and c-myc. ... TCE decreased methylation of the c-jun and c-myc genes and increased the level of their mRNAs. Decreased methylation of the protooncogenes could be a result of a deficiency in S-adenosylmethionine (SAM), so that methionine, by increasing the level of SAM, would prevent hypomethylation of the genes. For 5 days, female B6C3F1 mice were administered, daily by oral gavage, either 1000 mg/kg bw of TCE or 500 mg/kg DCA or TCA. At 30 min after each dose of carcinogen, the mice received, by ip injection, 0, 30, 100, or 450 mg/kg methionine. Mice were euthanized at 100 min after the last dose of DCA, TCA, or TCE. Decreased methylation in the promoter regions of the c-jun & c-myc genes and increased levels of their mRNA and proteins were found in livers of mice exposed to TCE, DCA, and TCA. Methionine prevented both the decreased methylation & the increased levels of the mRNA and proteins of the two protooncogenes. The prevention by methionine of DCA- TCA-, and TCE-induced DNA hypomethylation supports the hypothesis that these carcinogenes act by depleting the availability of SAM. Hence, methionine would prevent DNA hypomethylation by maintaining the level of SAM. Furthermore, the results suggest that the dose of DCA, TCA, or TCE must be sufficient to decrease the level of SAM in order for these carcinogens to be active.
PMID:10774822 Tao L et al; Toxicological Sciences 54 (2): 399-407 (2000)
Kidney tumors (renal-cell carcinomas) from workers occupationally exposed to high levels of TCE exhibited somatic mutations of the von Hippel-Landau (VHL) tumor suppressor gene, a gene that has been associated with renal-cell carcinoma. Mutations in the VHL gene were found in 75% of renal-cell carcinomas from 44 TCE-exposed persons. DNA sequencing analysis showed that 39% of these tumors had a specific mutation, a C to T transition at nucleotide (nt) 454, resulting in a Pro to Ser amino acid change at codon 81. In four patients, the nt 454 mutation also was found in the nearby noncancerous kidney tissue. Moreover, this mutation was specific to TCE exposure, because it was not found in renal-cell carcinomas from patients not exposed to TCE, and it was related to the disease, because it was not found in germline DNA from either diseased or nondiseased individuals. It is reasonable from a biological perspective that the kidney tumors observed in humans are related to TCE exposure because (1) the site and histopathological characteristics of the tumors in humans and experimental animals are similar, (2) a portion of the molecular mechanism of this type of cancer (nephrocarcinogenicity) has been discovered, (3) the metabolites derived from TCE (the likely ultimate electrophilic intermediates of its bioactivation) are identical in humans and experimental animals, and (4) taking the key urinary metabolites (mercapturic acids) as an indicator of the bioactivation of TCE, humans seem to be more sensitive than rats in developing the primary biochemical lesion that precedes kidney cancer.
DHHS/National Toxicology Program; Eleventh Report on Carcinogens: Trichloroethylene (79-01-6) (January 2005). Available from, as of September 10, 2010: https://ntp.niehs.nih.gov/ntp/roc/eleventh/profiles/s180tce.pdf
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