Disease relevance of Ethinyl trichloride

• Trichloroethylene exposure and specific somatic mutations in patients with renal cell carcinoma [1].
• Chronic dysphagia and trigeminal anesthesia after trichloroethylene exposure [2].
• The methanotrophic bacterium Methylosinus trichosporium 0B3b degrades trichloroethylene more rapidly than other bacteria examined to date [3].
• A recombinant Escherichia coli strain expressing hybrid Dox that had replaced BphA1 with TodC1 (alpha subunit of toluene dioxygenase (TolDox) of Pseudomonas putida) exhibited high activity toward trichloroethylene (TCE) (Furukawa, K., Hirose, J., Hayashida, S., and Nakamura, K. (1994) J. Bacteriol. 176, 2121-2123) [4].
• Renal toxicity and carcinogenicity of trichloroethylene: key results, mechanisms, and controversies [5].

Psychiatry related information on Ethinyl trichloride

• Previous work showed that trichloroethylene (TCE) impairs sustained attention as evidenced by a reduction in accuracy and elevation of response latencies in rats trained to perform a visual signal detection task (SDT) [6].
• Modification of auditory evoked startle responding using prepulse inhibition was used to examine the effects of trichloroethylene (TCE) exposure on auditory thresholds [7].
• Time-dependent effects of trichloroethylene on motor activity in rats [8].
• The effect of 2 mM ethanol, a concentration indicative of daily alcohol consumption, was investigated on trichloroethylene (TRI) metabolism in perfused Wistar rat liver [9].
• It is found that TCE concentration, vegetable yield, deposition interception fraction of vegetables, and plant surface loss constant, are the four parameters important to the decision-making of the case problem [10].

High impact information on Ethinyl trichloride

• BACKGROUND: The development of renal cell carcinoma (RCC) has been associated with both genetic and environmental factors-with mutations in the von Hippel-Lindau (VHL) tumor suppressor gene for clear-cell RCC specifically and with long-term exposure to high doses of trichloroethylene (TRI), an industrially important solvent, for RCC generally [1].
• We conclude that trichloroethylene potentiates the hepatotoxicity of carbon tetrachloride, possibly by increasing carbon tetrachloride-induced lipid peroxidation [11].
• Previous administration of carbon tetrachloride failed to modify lipid peroxidation and to increase the hepatotoxicity of trichloroethylene [11].
• Liver histology was normal 24 h after the administration of trichloroethylene (1 ml . kg-1) in rats [11].
• Reversion events in premelanocytes in the mouse embryo detected as black spots on the gray fur of the offspring were inducible by the carcinogen x-rays, ethyl methanesulfonate, methyl methanesulfonate, ethyl nitrosourea, benzo[a]pyrene, trichloroethylene, benzene, and sodium arsenate [12].

Chemical compound and disease context of Ethinyl trichloride

• During an informal study in 1973 it was noted that approximately one third of patients with congenital heart disease lived in a small area in the Tucson Valley. In 1981 groundwater for a nearly identical area was found to be contaminated with trichloroethylene and to a lesser extent with dichloroethylene and chromium [13].
• Possible involvement of glutathione and p53 in trichloroethylene- and perchloroethylene-induced lipid peroxidation and apoptosis in human lung cancer cells [14].
• Although it is not clear if the clinically administered dosage of chloral hydrate or the relatively high environmental levels of trichloroethylene could lead to an onset of Parkinson's disease, the spontaneous in vivo formation of TaClo and its pro-apoptotic properties, as shown in this report, should be considered [15].
• In contrast, indirect toxicants that elicit an immune-mediated toxicity such as halothane, and possibly diclofenac and trichloroethylene, appear to have a limited number of protein targets with a high substitution level, and the immune system is exposed repeatedly to the modified proteins [16].
• Given the demonstrated phenol-dependent trichloroethylene (TCE) degradation in Alcaligenes eutrophus JMP134 (A. R. Harker and Y. Kim, Appl. Environ. Microbiol. 56:1179-1181, 1990), this work represents a purposeful effort to create a constitutive degrader of TCE [17].

Biological context of Ethinyl trichloride

• Trichloroethylene and dichloroethylene administered during organogenesis are cardiac, but not general, teratogens [18].
• These results suggest that trichloroethylene treatment causes a male-specific PPARalpha-dependent increase in cellular oxidative stress [19].
• The mechanism of trichloroethylene-induced liver peroxisome proliferation and the sex difference in response was investigated using wild-type Sv/129 and peroxisome proliferator-activated receptor alpha (PPARalpha)-null mice [19].
• ras proto-oncogene activation in dichloroacetic acid-, trichloroethylene- and tetrachloroethylene-induced liver tumors in B6C3F1 mice [20].
• Trichloroethylene, given by gavage and inhalation, was carcinogenic in the B6C3F1 mice [21].

Anatomical context of Ethinyl trichloride

• The metabolism of the suspected carcinogen trichloroethylene (TCE) was studied in in vitro systems involving purified rat liver cytochrome P-450; rat, human, and mouse liver microsomes; rat lung microsomes; and isolated rat and mouse hepatocytes [22].
• Covalent interaction of metabolites of the carcinogen trichloroethylene in rat hepatic microsomes [23].
• After trichloroethylene exposure of rats, renal cell tumors were found increased in males, and an increased incidence of interstitial cell tumors of the testes was reported [5].
• Epidemiological cohort studies addressing the carcinogenicity of trichloroethylene with respect to the renal or urothelial target sites have been conducted, and no clear evidence for an elevated renal or urinary tract cancer risk in trichloroethylene-exposed groups was visible in exposed populations [5].
• Further investigations on patients with renal cell carcinoma and with histories of high trichloroethylene exposures, on the basis of excretion of marker proteins in the urine, pointed to toxic damage to the proximal renal tubules by trichloroethylene [5].

Associations of Ethinyl trichloride with other chemical compounds

• A key question in the risk assessment of trichloroethylene (TRI) is the extent to which its carcinogenic effects might depend on the formation of dichloroacetate (DCA) as a metabolite [24].
• Mutations at codons 13 and 117 plus a second exon insert contributed 4% to the total H-ras frequencies for trichloroethylene and tetrachloroethylene [20].
• On the other hand, trichloroethylene induced liver cytochrome P450 2E1, the principal enzyme responsible for metabolizing trichloroethylene to chloral hydrate, only in males, which resulted in similar expression levels in both sexes after the treatment [19].
• The mutation spectra of H-ras codon 61 mutations showed a significant decrease in AAA and increase in CTA mutations for dichloroacetic acid- and trichloroethylene-induced tumors when compared to combined controls [20].
• Nitrogen-doped TiO2 has been used to investigate mechanistically the photocatalytic oxidation of trichloroethylene (TCE) under irradiation with visible light (lambda > or = 420 nm) [25].

Gene context of Ethinyl trichloride

• This contrasts with a recent report of reduced risk of RCC associated with GSTT1 null in a cohort of trichloroethene-exposed workers and suggests that specific chemical exposures alter the effect of GSTT1 on cancer risk [26].
• Differences in cytochrome P450-catalysed oxidation of benzene, toluene and trichloroethylene (TRI) between male Wistar rats and male B6C3F1 mice were investigated by immunoblot and immunoinhibition assays using monoclonal antibodies (MAbs) to cytochrome P450 (CYP1A1/2, CYP2B1/2, CYP2E1 and CYP2C11/6) [27].
• Taken collectively, metabolism of trichloroethylene by CYP2E1 is responsible, at least in part, for the CD4+ T cell alterations associated with exposure to this environmental toxicant [28].
• Exposure to a metabolite of the environmental toxicant, trichloroethylene, attenuates CD4+ T cell activation-induced cell death by metalloproteinase-dependent FasL shedding [29].
• Although this polymorphism is limited in the case of Japanese as well as other Asian subjects, the inhibitors of ALDH2 activity such as trichloroethylene may produce a false polymorphism of this gene [30].

Analytical, diagnostic and therapeutic context of Ethinyl trichloride

• This study confirmed the results of the previous cohort study, supporting the concept of involvement of prolonged and high-dose trichloroethylene exposures in the development of renal cell cancer [5].
• We examined the effects of trichloroethylene (TCE) on the bronchiolar epithelium of mouse lung, using scanning electron microscopy [31].
• The model presents results that cast doubt on the practicality of using methane or propane for the co-metabolic destruction of trichloroethylene in a gas phase bioreactor [32].
• TCE has been implicated as a cardiac teratogen in an epidemiologic study and in a chick model [33].
• In lifetime bioassays, trichloroethylene (TCE, CAS No. 79-01-6) causes liver tumors in mice following gavage, liver and lung tumors in mice following inhalation, and kidney tumors in rats following gavage or inhalation [34].

References