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At least 19 recordsLinked to original sources
PubMed1994

The glycolic acid trichloroacetic acid peel.

BACKGROUND: Chemical peeling has become increasingly popular. Technique is more critical in medium depth peeling than with deeper peels because of variable penetration of the trichloroacetic acid. OBJECTIVE: This article describes a novel use of two caustic agents, glycolic acid and trichloroacetic acid, to effect a predictable approach to medium depth peeling. METHODS: Without other skin preparation, 70% glycolic acid was applied to the entire face and diluted with water after 2 minutes. Then, 35% trichloroacetic acid was applied over the same areas. Biopsies were done on selected patients after 24 hours and 30, 60, and 90 days. RESULTS: Both clinically and histologically the glycolic trichloroacetic acid peel resulted in medium depth injury. Improvement in pigmentary dyschromias and actinic damage was impressive. CONCLUSION: The GA-TCA peel provides a consistent approach to medium depth peeling to add to the armamentarium of the dermatologic surgeon.

Adult↗
PubMed1978

Measurement of polyadenylic acid by hybridization with polyuridylic acid: a source of error due to the lability of tritiated polyuridylic acid in trichloroacetic acid.

During brief exposure to trichloroacetic acid at 0 degree C, significant amounts of tritiated polyuridylic acid are converted to acid-soluble products. The loss of polymeric radioactivity is dependent on both acid concentration and the time of exposure to acid. When trichloroacetic acid precipitation is used to recover the tritiated polyuridylic acid present in a hybrid with polyadenylic acid, significant underestimates of the hybridized radioactivity can occur because of the lability of tritiated polyuridylic acid. Conditions are given which minimize the lability and permit quantitative recovery of tritiated polyuridylic acid by trichloroacetic acid precipitation.

Chemical Precipitation↗
PubMed2003

Long-term exposure of Sitka spruce seedlings to trichloroacetic acid.

Trichloroacetic acid (TCA) has been implicated as an airborne pollutant responsible for adverse effects on forest health. There is considerable debate as to whether TCA observed in trees and forest soils is derived from atmospheric deposition or from in situ production. This experiment reports the results from treating 4-year-old Sitka spruce (Picea sitchensis (Bong.) Carr) plants in a greenhouse over a growing season with TCA supplied either to the soil or to the foliage at concentrations of 10 and 100 ng mL(-1). Similar uptake of TCA by needles was observed for both modes of treatment, with significant accumulation of TCA (300 ng g(-1) dry wt) at the higher concentration. Larger concentrations in stem tissue were seen for the foliar-applied TCA (280 ng g(-1)) than for the soil-applied TCA (70 ng g(-1)), suggesting that direct stem uptake may be important. Six months after treatments stopped, TCA concentrations in the needles of plants exposed to 100 ng mL(-1) TCA were still enhanced, showing that biological degradation of TCA in needles was slow over the winter. By contrast, no significant enhancement of TCA in soil could be detected in the directly treated soils even during the experiment. The protein content of needles treated with the higher concentration of TCA by either route was significantly smaller than for the controls, but there was no effect of TCA on the conjugation of 1-chloro-2,4-dinitrobenzene in roots nor on the conjugation of 1,2-dichloro-4-nitrobenzene in needles.

Biodegradation, Environmental↗
PubMed1980

Consideration of the evidence for mechanisms of 1,1,2-trichloroethylene metabolism, including new identification of its dichloroacetic acid and trichloroacetic acid metabolites in mice.

Data derived from studies with vinylidene chloride (1,1-dichloroethylene)and 1,1,2-trichloroethylene suggest that similar mutagenic and tumorogenic properties in mice may be attributable to rearrangement of the 2 haloalkene-derived haloepoxides, respectively, into chloroacetyl chloride and dichloroacetyl chloride. On the other hand, the relative harmlessness of 1,1,2-trichloroethylene in rats and man is due to alternative rearrangement of 1,1,2-trichloroethylene oxide into chloral and the further products of its metabolism. The identification in mice of the new 1,1,2-trichloroethylene metabolite, dichloroacetic acid (in addition to trichloroacetic acid) strongly supports this supposition. The small proportion of dichloroacetic acid in relation to the large proportion of trichloroacetic acid in the urine of the treated mice is consistent with a spill-over model that is now tentatively proposed for 1,1,2-trichloroethylene metabolism in these animals.

Acetates↗
PubMed1996

Carcinogenic activity of dichloroacetic acid and trichloroacetic acid in the liver of female B6C3F1 mice.

The concentration-response relationships for the hepatocarcinogenic activity of dichloroacetic acid2 (DCA) and trichloroacetic acid (TCA), two contaminants of finished drinking water, were determined in female B6C3F1 mice. Dicholoracetic acid or trichloroacetic acid at 2.0, 6.67, or 20.0 mmol/liter was administered to the mice in the drinking water starting at 7 to 8 weeks of age and until sacrifice after 360 or 576 days of exposure. The relationships of the yield of foci of altered hepatocytes, hepatocellular adenomas, and hepatocellular carcinomas to the concentration of DCA and TCA in the water were best described by second-order and linear regressions, respectively. The liver-to-body weight ratio increased linearly for both DCA and TCA, as did the vacuolization of the liver induced by DCA. The foci of altered hepatocytes and tumors in the animals treated with DCA were predominantly eosinophilic and contained glutathione S-transferase-pi (GST-pi, over 80% of the lesions), while the tumors induced by TCA were predominantly basophilic and lacked GST-pi, including all 11 hepatocellular carcinomas. Therefore, the carcinogenic activity of DCA AND TCA appeared to differ both with respect to their dose- response relationship and to the characteristics of precancerous lesions and tumors.

Animals↗
PubMed2000

Determination of dichloroacetic acid and trichloroacetic acid by liquid-liquid extraction and ion chromatography.

An extraction technique using MTBE (methyl tert. butyl ether) and reagent water in combination with ion chromatography and conductivity determination was developed to quantify dichloroacetic acid (DCAA) and trichloroacetic acid (TCAA) concentrations in raw water after chlorination. The detection limit of the method was 0.45 and 1.50 microg/L for DCAA and TCAA, respectively. Mean values of recovery ranged from 90 to 96% for DCAA and 95 to 108% for TCAA. The evaluation of recovery and precision of the method indicates that the performance characteristics are comparable with gas chromatographic (GC) methods reported in literature. In addition, the procedure is simple, fast, and does not need any derivatization step. Application of the analytical method to the determination of DCAA and TCAA in real samples is shown.

Chlorine↗
PubMed1998

Effect of dichloroacetic acid and trichloroacetic acid on DNA methylation in liver and tumors of female B6C3F1 mice.

Dichloroacetic acid (DCA) and trichloroacetic acid (TCA) are found in drinking water and are metabolites of trichloroethylene. They are carcinogenic and promote liver tumors in B6C3F1 mice. Hypomethylation of DNA is a proposed nongenotoxic mechanism involved in carcinogenesis and tumor promotion. We determined the effect of DCA and TCA on the level of DNA methylation in mouse liver and tumors. Female B6C3F1 mice 15 days of age were administered 25 mg/kg N-methyl-N-nitrosourea and at 6 weeks started to receive 25 mmol/liter of either DCA or TCA in their drinking water until euthanized 44 weeks later. Other animals not administered MNU were euthanized after 11 days of exposure to either DCA or TCA. DNA was isolated from liver and tumors, and after hydrolysis 5-methylcytosine (5MeC) and the four bases were separated and quantitated by HPLC. In animals exposed to either DCA or TCA for 11 days but not 44 weeks, the level of 5MeC in DNA was decreased in the liver. 5MeC was also decreased in liver tumors from animals exposed to either chloroacetic acid. The level of 5MeC in TCA-promoted carcinomas appeared to be less than in adenomas. Termination of exposure to DCA, but not to TCA, resulted in an increase in the level of 5MeC in adenomas to the level found in noninvolved liver. Thus, hypomethylated DNA was found in DCA and TCA promoted liver tumors and the difference in the response of DNA methylation to termination of exposure appeared to support the hypothesis of different mechanisms for their carcinogenic activity.

5-Methylcytosine↗
PubMed1997

Promotion by mixtures of dichloroacetic acid and trichloroacetic acid of N-methyl-N-nitrosourea-initiated cancer in the liver of female B6C3F1 mice.

Hepatic tumor promoting activity was determined for mixtures of dichloroacetic acid (DCA) and trichloroacetic acid (TCA) in female B6C3F1 mice initiated on day 15 of age with 25 mg/kg N-methyl-N-nitrosourea. The mice received in their drinking water from 6 to 50 weeks of age either DCA (7.8, 15.6, or 25 mmol/l) with/without 6.0 mmol/l TCA or TCA (6.0 or 25 mmol/l) with/without 15.6 mmol/l DCA. Proliferative lesions (foci of altered hepatocytes and hepatocellular adenomas) promoted by TCA increased linearly with its concentration and were predominantly basophilic and negative for glutathione S-transferase-pi (GST-pi), while those promoted by DCA increased exponentially with its concentration and were eosinophilic and positive for GST-pi. The promoting activity of DCA and TCA in mixtures was at least additive. The proliferative lesions resulting from exposure to the mixtures were predominately similar to those promoted by DCA, i.e. contained eosinophilic and GST-pi-positive hepatocytes.

Animals↗
PubMed1996

Promotion by dichloroacetic acid and trichloroacetic acid of N-methyl-N-nitrosourea-initiated cancer in the liver of female B6C3F1 mice.

Hepatic tumor promoting activity was determined for dichloroacetic acid (DCA) and trichloroacetic acid (TCA) in female B6C3F1 mice initiated on day 15 of age with 25m/kg N-methyl-N-nitrosourea (MNU). The mice were administered the chloroacetic acids in drinking water starting at 7 weeks of age and continuing until sacrificed 31 or 52 weeks later. Both chloroacetic acids promoted MNU-initiated foci and tumors, however their concentration-response relationships differed being exponential and linear for DCA or TCA, respectively. Lesions promoted by DCA but not by TCA, regressed upon termination of exposure at 31 weeks. Foci and tumors promoted by DCA were eosinophilic and contained glutathione S-transferase-pi(GST-pi), while TCA promoted basophilic tumors lacking GST-pi. Hence, tumor promotion by DCA and TCA appeared to differ both with respect to their concentration-response relationships and to the characteristics of precancerous lesions and tumors.

Animals↗
PubMed2001

The effect of dichloroacetic acid and trichloroacetic acid on DNA methylation and cell proliferation in B6C3F1 mice.

The chlorine disinfection by-products, dichloroacetic acid (DCA) and trichloroacetic acid (TCA), are carcinogenic in mouse liver. We have previously reported that DCA and TCA induced DNA hypomethylation in mouse liver. In the present study, we determined the temporal association for DNA hypomethylation and cell proliferation. Female B6C3F1 mice were administered daily doses of 500 mg/kg DCA or TCA by gavage and sacrificed at 24, 36, 48, 72, and 96 hours after the first dose. The proliferating cell nuclear antigen-labeling index in the liver was increased at 72 and 96 hours by both DCA and TCA, that is, at 72 hours the index was 1.00 +/- 0.21, 0.51 +/- 0.11, and 0.095 +/- 0.016 for DCA, TCA, and the vehicle control, respectively. The mitotic index was also significantly increased at 96 hours. The promoter region for the c-myc gene was hypomethylated only at 72 and 96 hours and not at the earlier sacrifices. Similarly, the methylation of the c-myc gene in the kidney and urinary bladder was decreased only at 72 and 96 hours. In summary, enhancement of cell proliferation and decreased methylation of the c-myc gene were first observed simultaneously at 72 hours after the start of exposure. Thus, the results support the hypothesis that DCA and TCA induce DNA hypomethylation by inducing DNA replication and preventing the methylation of the newly synthesized strands of DNA.

Animals↗
PubMedDate not supplied

Dissimilar characteristics of N-methyl-N-nitrosourea-initiated foci and tumors promoted by dichloroacetic acid or trichloroacetic acid in the liver of female B6C3F1 mice.

Dichloroacetic acid (DCA) and trichloroacetic acid (TCA) are metabolites of the industrial solvent and environmental contaminant trichloroethylene (TCE), as well as contaminants of chlorinated drinking water. Human exposure to these chemicals is of concern as all three have been shown to increase liver tumor incidence in mice. Differences in dose-response curves, progression to cancer, and postexposure regression of lesions suggest that TCA and DCA work through different mechanisms. The purpose of this study was to further characterize the proliferative hepatocellular lesions promoted by TCA and DCA using biomarkers of cell growth, differentiation, and metabolism in liver sections to better delineate the distinctions in the mechanism of the two chloroacetates. Fifteen-day-old female mice were initiated with 25 mg/kg N-methyl-N-nitrosourea. The initiated mice were administered DCA or TCA (20.0 mmol/L) in drinking water from age 49 days until euthanasia at age 413 days. The pathologic assessment showed that the foci of altered hepatocytes and tumors occurring in the animals promoted with DCA were eosinophilic and positive immunohistochemically for TGF-alpha, c-jun, c-myc, CYP 2E1, CYP 4A1, and glutathione S-transferase-pi (GST-pi). The DCA lesions also were essentially negative for c-fos and TGF-beta, but nontumor hepatocytes were consistently TGF-beta-positive. In contrast, tumors promoted by TCA were predominantly basophilic, lacked GST-pi, and stained variably; usually, more than 50% of the tumor hepatocytes were essentially negative for the other biomarkers. This study demonstrates some striking differences in certain molecular biomarkers of cell growth, differentiation, and metabolism between DCA and TCA. The results also suggest some potential growth signal transduction pathways that may contribute to the DCA promotion of tumors, further support the premise that these two chloroacetates promote hepatocarcinogenesis in different ways, and provide a rational basis for a similar comparison with TCE. Such a comparison should give some insight as to whether DCA, TCA, or both are playing a significant role in the murine liver carcinogenesis of the parent compound, TCE.

Animals↗
PubMed2000

Effect of trichloroethylene and its metabolites, dichloroacetic acid and trichloroacetic acid, on the methylation and expression of c-Jun and c-Myc protooncogenes in mouse liver: prevention by methionine.

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. We have previously reported that 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 body weight 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-, 300-, 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 and 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 and the increased levels of the mRNA and proteins of the two pro-tooncogenes. The prevention by methionine of DCA- TCA-, and TCE-induced DNA hypomethylation supports the hypothesis that these carcinogens 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.

Animals↗
PubMed1997

Failure of monochloroacetic acid and trichloroacetic acid administered in the drinking water to produce liver cancer in male F344/N rats.

The chlorinated acetic acids monochloroacetic acid (MCA) and trichloroacetic acid (TCA) are found as chlorine disinfection by-products in finished drinking-water supplies. TCA has been demonstrated to be a mouse liver carcinogen. A chronic study in which male Fischer 344/N rats were exposed for 104 wk to TCA and MCA in the drinking water is described. Animals, 28 d old, were exposed to 0.05, 0.5, or 2 g/L MCA, or 0.05, 0.5, or 5 g/L TCA. The 2.0 g/L MCA was lowered in stages to 1 g/L when the animals began to exhibit signs of toxicity. A time-weighted mean daily MCA concentration (MDC) of 1.1 g/L was calculated over the 104-wk exposure period. Time-weighted mean daily doses (MDD) based upon measured water consumption were 3.5, 26.1, and 59.9 mg/kg/d for 0.05, 0.5, and 1.1 g/L MCA, respectively; TCA MDD were 3.6, 32.5, and 363.8 mg/kg/d. Nonneoplastic hepatic changes were for the most part spontaneous and age related. No evidence of hepatic neoplasia was found at any of the MCA or TCA doses. The incidence of neoplastic lesions at other sites was not enhanced over that in the control group. Drinking water concentrations of > or = 0.5 g/L MCA produced a moderate to severe toxicity as reflected by a depressed water consumption and growth rate. A no-observed-effects level (NOEL) for carcinogenicity of 0.5 g/L (26.1 mg/kg/d) MCA was calculated. TCA at drinking water levels as high as 5 g/L produced only minimal toxicity and growth inhibition and provided a NOEL of 364 mg/kg/d. Our results demonstrate that under the conditions of this bioassay, MCA and TCA were not tumorigenic in the male F344/N rat.

Acetates↗
PubMed1992

Dichloroacetic acid and trichloroacetic acid increase chloroform toxicity.

Dichloro- and trichloroacetic acids (DCA and TCA) and chloroform are formed during chlorination disinfection of drinking water. The effects of DCA and TCA treatment on CHCl3 toxicity were assessed in these studies. Male and female rats were gavaged with DCA or TCA (0.92 and 2.45 mmol/kg administered 3 times over 24 h). Three hours after the last dose CHCl3 was injected ip (0.75 mg/kg). Male rats experienced some weight loss (15%) and slight increases of ALT and BUN, but there were no effects of either DCA or TCA on any of these responses. In females, CHCl3 increased plasma ALT and this response was greater (up to threefold) in the DCA group, compared to saline controls. Similarly, BUN was increased by CHCl3 and this was more severe (up to threefold) in both the DCA and TCA pretreated groups. These results show that CHCl3 toxicity is increased by DCA and TCA, and this effect is gender-specific, occurring only in females. DCA increases both liver and kidney toxicity, whereas TCA affects only kidney toxicity.

Alanine Transaminase↗
PubMed1976

Trichloroacetic acid peeling.

Trichloroacetic acid peeling refers to a system whereby a corrosive chemical is applied to the skin. The resultant good effect is due to epidermal regeneration, as well as the regenerating of new collagen in the dermis. The technique of deep chemical peeling in treatment of actinic degeneration and acne scarring is presented.

Chemexfoliation↗