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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↗
PubMed2002

Chemical injury to the eye from trichloroacetic Acid.

BACKGROUND: Trichloroacetic acid (TCA) is frequently utilized for chemical peeling by physicians practicing dermatologic surgery. Ocular complications from TCA have not been reported previously. OBJECTIVE: The purpose of this article is to underscore the irritating and corrosive effects of TCA on the eye. METHODS: A patient is described who experienced seepage of 35% TCA into the eye during a chemical peel. RESULTS: The patient developed marked conjunctivitis of the affected eye and abrasions involving 25% of the cornea. CONCLUSION: TCA must be applied carefully around the eyes to avoid ocular complications, which albeit rare, can be quite grave if not addressed in a timely manner.

Chemexfoliation↗
PubMedDate not supplied

Some effects of replacement of metaphosphoric acid/acetic acid solvent system with trichloroacetic acid in microfluorometric determination of vitamin C.

Trichloroacetic acid (TCA) is suggested as a substitute for the metaphosphoric acid/acetic acid (HPO3-HOAc) solvent system in the AOAC microfluorometric determination of vitamin C. Comparative advantages of TCA are easier handling, greater stability, and the approximate 10-fold increase in sensitivity. For both solvent systems, the influence of acid concentration on fluorescence is described. TCA provides maximum fluorescence enhancement at pH 5.5-6.0.

Acetates↗
PubMed1996

A clinical and histologic evaluation of two medium-depth peels. Glycolic acid versus Jessner's trichloroacetic acid.

BACKGROUND: Chemical peels using alpha hydroxy acids have become one of the most frequently requested dermatologic procedures. The use of glycolic acid in superficial chemical peels is now well established. However, the role of glycolic acid in medium-depth chemical peels has yet to be elucidated. OBJECTIVE: We performed a clinical and histologic comparison of 70% glycolic acid versus Jessner's solution as part of a medium-depth chemical peel using 35% trichloroacetic acid (TCA). METHODS: Thirteen patients with actinic keratoses, solar lentigines and fine wrinkling were evaluated prospectively. Each patient was treated with 70% glycolic acid plus 35% TCA (GA-TCA) to the right face and Jessner's solution plus 35% TCA (JS-TCA) to the left face. Clinical and histologic changes were evaluated at 7, 30, and 60 days postoperatively. RESULTS: Clinically, the GA-TCA peel was effective in treating photodamaged skin. The GA-TCA peel was slightly more efficacious in removing actinic keratoses (clinical response score = 1.5) than the JS-TCA peel (clinical response score = 1.0). Histologically, the GA-TCA peel caused the formation of a slightly thicker Grenz zone (mean = 0.053 mm) 60 days postpeel than the JS-TCA peel (mean = 0.048 mm) (not statistically significant). The GA-TCA peel caused more neoelastogenesis than the JS-TCA peel, while the JS-TCA peel resulted in more papillary dermal fibrosis and neovascularization than the GA-TCA peel. CONCLUSION: The GA-TCA peel is a new medium-depth chemical peel that is effective in treating photodamaged skin.

Chemexfoliation↗
PubMed1989

Characterization of the proteoglycogen fraction non-extractable from retina by trichloroacetic acid.

The trichloroacetic acid-insoluble 1,4-alpha-glucan fraction from bovine retina was purified and characterized. It is a proteoglycogen fraction containing a 42 kDa protein moiety similar in size to the protein moiety of the trichloroacetic acid-soluble proteoglycogen fraction. The apparent weight-average Mr of acid-insoluble and acid-soluble proteoglycogens are 4.7 x 10(5) and 7.0 x 10(5) respectively. The present results support suggestions from earlier studies indicating that acid-insoluble proteoglycogen is the precursor of the acid-soluble form.

Animals↗
PubMed1998

Mutagenicity of three disinfection by-products: di- and trichloroacetic acid and chloral hydrate in L5178Y/TK +/- (-)3.7.2C mouse lymphoma cells.

The disinfection of water, required to make it safe for human consumption, leads to the presence of halogenated organic compounds. Three of these carcinogenic 'disinfection by-products', dichloroacetic acid (DCA), trichloroacetic acid (TCA) and chloral hydrate (CH) have been widely evaluated for their potential toxicity. The mechanism(s) by which they exert their activity and the steps in the etiology of the cancers that they induce are important pieces of information that are required to develop valid biologically-based quantitative models for risk assessment. Determining whether these chemicals induce tumors by genotoxic or nongenotoxic mechanisms (or a combination of both) is key to this evaluation. We evaluated these three chemicals for their potential to induce micronuclei and aberrations as well as mutations in L5178Y/TK +/- (-)3.7.2C mouse lymphoma cells. TCA was mutagenic (only with S9 activation) and is one of the least potent mutagens that we have evaluated. Likewise, CH was a very weak mutagen. DCA was weakly mutagenic, with a potency (no. of induced mutants/microgram of chemical) similar to (but less than) ethylmethanesulfonate (EMS), a classic mutagen. When our information is combined with that from other studies, it seems reasonable to postulate that mutational events are involved in the etiology of the observed mouse liver tumors induced by DCA at drinking water doses of 0.5 to 3.5 g/l, and perhaps chloral hydrate at a drinking water dose of 1 g/l. The weight-of-evidence for TCA suggest that it is less likely to be a mutagenic carcinogen. However, given the fact that DCA is a weak mutagen in the present and all of the published studies, it seems unlikely that it would be mutagenic (or possibly carcinogenic) at the levels seen in finished drinking water.

Animals↗
PubMed2004

The ecological effects of trichloroacetic acid in the environment.

Trichloroacetic acid (TCAA) is a member of the family of compounds known as chloroacetic acids, which includes mono-, di- and trichloroacetic acid. The significant property these compounds share is that they are all phytotoxic. TCAA once was widely used as a potent herbicide. However, long after TCAA's use as a herbicide was discontinued, its presence is still detected in the environment in various compartments. Methods for quantifying TCAA in aqueous and solid samples are summarized. Concentrations in various environmental compartments are presented, with a discussion of the possible formation of TCAA through natural processes. Concentrations of TCAA found to be toxic to aquatic and terrestrial organisms in laboratory and field studies were compiled and used to estimate risk quotients for soil and surface waters. TCAA levels in most water bodies not directly affected by point sources appear to be well below toxicity levels for the most sensitive aquatic organisms. Given the phytotoxicity of TCAA, aquatic plants and phytoplankton would be the aquatic species to monitor for potential effects. Given the concentrations of TCAA measured in various soils, there appears to be a risk to terrestrial organisms. Soil uptake of TCAA by plants has been shown to be rapid. Also, combined uptake of TCAA from soil and directly from the atmosphere has been shown. Therefore, risk quotients derived from soil exposure may underestimate the risk TCAA poses to plants. Moreover, TCE and TCA have been shown to be taken up by plants and converted to TCAA, thus leading to an additional exposure route. Mono- and di-chloroacetic acids can co-occur with TCAA in the atmosphere and soil and are more phytotoxic than TCAA. The cumulative effects of TCAA and compounds with similar toxic effects found in air and soil must be considered in subsequent terrestrial ecosystem risk assessments.

Animals↗
PubMed1989

Trichloroacetic acid peels revisited.

Trichloroacetic acid (TCA) is a time-honored peeling agent that has no known systemic toxicity. Recent interest in reversing the effects of actinic damage has led to the utilization of combination therapies. Retinoic acid, solid CO2, pyruvic acid, Jessner's formula, and other agents have been used to increase the effectiveness of TCA and enhance peeling results. Repetitive peels with low concentrations of TCA can be effective for areas prone to scarring.

Administration, Topical↗
PubMed1997

A histopathological study of liver and kidney in male Wistar rats treated with subtoxic doses of t-butyl alcohol and trichloroacetic acid.

Tertiary butyl alcohol and trichloroacetic acid are known to be contaminants in drinking water. In order to evaluate the interactive toxicity of t-butyl alcohol with trichloroacetic acid, young male Wistar rats were dosed through water at a dose level of t-butyl alcohol (TBA)-0.5% (v/v), trichloroacetic acid (TCA)-25 ppm and a combined dose of TBA + TCA (0.5% v/v TBA-25 ppm TCA) for a period of 10 weeks ad libitum and were maintained on normal diet. The control animals received plain water and normal diet. The liver and kidney histology was undertaken to see whether subtoxic administration of TBA and TCA individually as well as combined administration for a period of 10 weeks would bring about any histological alterations. It was observed that TBA, TCA and TBA + TCA caused histological alterations in the liver such as centrilobular necrosis, vacuolation in hepatocytes and loss of hepatic architecture. TBA and TBA + TCA caused periportal proliferation and lymphocytic infiltration. Hypertrophy of hepatocytes in the periportal area was a characteristic feature in the liver of TCA treated rats. Moreover, in the histology of the kidney, in the three treated groups, degeneration of renal tubules, with syncitial arrangements of the nucleus of renal tubular epithelial cells was evident. In addition to this, degeneration of the basement membrane of the Bowmans capsule, diffused glomeruli and vacuolation of glomeruli was also evident in the three treated rat kidneys. Renal tubular proliferation in certain areas was also evident in certain areas of the kidney in TCA treated rats. The results indicate that, TBA and TCA do bring about alterations in histology of liver and kidney, but on combined administration, do not show enhanced toxicity in the form of increased hepatic and renal injury.

Animals↗
PubMed1983

Denaturation studies on bovine pancreatic ribonuclease. Effect of trichloroacetic acid.

Exposure of ribonuclease (EC 3.1.27.5) to 5% trichloroacetic acid solution is found to partially inactivate the enzyme. This inactivation is a function of time of exposure to trichloroacetic acid and reaches a plateau of about 45% residual activity. Higher concentrations of trichloroacetic acid lead to greater inactivation. Physicochemical properties such as sedimentation coefficient, gel-filtration behaviour and polyacrylamide gel electrophoresis of the trichloroacetic acid-treated enzyme remain unaffected as compared to the untreated enzyme. However, spectrophotometric titration of the trichloroacetic acid-treated enzyme revealed that one of the three 'buried' groups of tyrosine is exposed to the outside surface of the molecule. Near ultraviolet CD spectra supported these observations. Far ultraviolet CD spectra suggested some refolding of the enzyme after trichloroacetic acid treatment. Immunological determinants on the molecule remain unaltered upon trichloroacetic acid treatment. It is concluded that the exposed tyrosine group may be causing a conformational change in the protein and this change may be indirectly responsible for the observed reduction in the activity after trichloroacetic acid treatment.

Animals↗
PubMed2000

Formulation of trichloroacetic acid peeling solution: a bibliometric analysis.

Since the beginning of this century, trichloroacetic acid solutions of various concentrations have been used for chemical exfoliation. These solutions have been prepared by using four different formulas. To prepare a 50% solution, for instance, water may be added to 50 g of trichloroacetic acid crystals until 100 ml of solution is obtained (weight-to-volume solution). Alternatively, 50 g of water may be added to 50 g of trichloroacetic acid crystals (weight-to-weight solution), or 50 g of trichloroacetic acid crystals may be solved in 100 ml of water (weight-plus-volume solution). Finally, a saturated trichloroacetic acid solution (or "100% solution") may be diluted by an equal volume of water (dilution). Depending on the method used, these so-called 50% solutions contain 40 to 71 weight-to-volume percentages of trichloroacetic acid. From a review of 120 publications on trichloroacetic acid peeling that have appeared since 1926, it was concluded that the authors of 87 of these publications (73 percent) did not report their formula for the trichloroacetic acid solution. Any one of the four methods was reported to have been used by the 33 authors who did report their formula. Eight of 10 internationally reputed pharmacopeias were found not to include the formula of a trichloroacetic acid solution. Proper evaluation of results and prevention of complications of trichloroacetic acid chemexfoliation is only feasible if both the concentration and the formula of trichloroacetic acid solution are reported by the author. Practitioners who use a trichloroacetic acid solution need to establish that the concentration of the solution they apply corresponds with that of the solution reported in the literature.

Bibliometrics↗
PubMed2005

A review of analytical methods for the determination of trichloroethylene and its major metabolites chloral hydrate, trichloroacetic acid and dichloroacetic acid.

Trichloroethylene (TCE) and some of its metabolites are potentially carcinogenic compounds that the general population is commonly exposed to in drinking water. Concentrations of TCE, dichloroacetic acid (DCA) and trichloroacetic acid (TCA) given to laboratory animals in cancer bioassays are high, whereas drinking water levels of the compounds are very low. It is not clear whether the trace amounts of TCE, DCA and TCA in drinking water pose a cancer risk to humans. The accuracy of pharmacokinetic studies relies on the analytical method from which blood and tissue concentration data are obtained. Models that extrapolate cancer risks of TCE and its metabolites from laboratory animals to humans, in turn, rely on the results of pharmacokinetic studies. Therefore, it is essential to have reliable analytical methods for the analysis of TCE and its metabolites. This paper reviews the methods currently in the literature for the analysis of TCE, DCA, TCA and, to a lesser extent, chloral hydrate (CH). Additional aspects of analytical methods such as method validation, species preservation and future directions in the analysis of TCE and its metabolites are also discussed.

Animals↗
PubMed1997

Enterohepatic recirculation of trichloroethanol glucuronide as a significant source of trichloroacetic acid. Metabolites of trichloroethylene.

Trichloroacetic acid (TCA) is a metabolite of trichloroethylene (TRI) thought to contribute to its hepatocarcinogenic effects in mice. Recent studies have shown that peak blood concentrations of TCA do not occur until approximately 12 hr after an oral dose of TRI; however, blood concentrations of TRI reach a maximum within 1 hr and is nondetectable after 2 hr. The objective of this study was to examine quantitatively enterohepatic recirculation of trichloroethanol (TCEOH) and TCA as a possible mechanism responsible for the delayed production of TCA. Jugular vein, duodenum, and bile duct-cannulated Fischer 344 rats were used, with the collection of blood, bile, urine, and feces samples after intraduodenal and intravenous dosing of animals with TRI, TCEOH, and TCA. Samples were analyzed by GC for TCA, total TCEOH, and free TCEOH. The results show that, after an intravenous dose of TCEOH (100 mg/kg), 36% of the TCEOH in blood is attributable to enterohepatic recirculation. With the same treatment, 76% of the TCA in blood is attributable to enterohepatic recirculation of metabolites. Peak concentrations of total TCEOH in bile, after an intraduodenal dose of TRI, are over 5 times higher than peak concentrations of total TCEOH in systemic blood. Peak concentrations of TCEOH glucuronide in bile are approximately 200 times higher than peak concentrations of TCEOH glucuronide in systemic blood.

Animals↗