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PubMed1989

Teratogenic activity of trichloroacetic acid in the rat.

Trichloroacetic acid (TCA) is a by-product of the chlorine disinfection of water containing natural organic material. It is detectable in finished drinking water at levels comparable to the trihalomethanes (30-160 micrograms/L). TCA is also formed in vivo after ingestion of hypochlorite and has been identified as a major metabolite of chlorinated hydrocarbons such as trichloroethylene. The developmental effects of TCA were evaluated in the pregnant Long-Evans rat. Animals were dosed by oral intubation on gestation days 6-15 (plug = 0) with 0, 330, 800, 1,200, or 1,800 mg/kg/day. The vehicle control was distilled water. Maternal observations included clinical signs, weight change, and gross evaluation of organ weights and uterine contents at necropsy (day 20). Live fetuses were examined for external, skeletal, and soft tissue malformation. There were no maternal deaths associated with toxicity prior to sacrifice. Weight gain during treatment was reduced at 800, 1,200, and 1,800 mg/kg. Spleen and kidney weights were increased in a dose-related manner. The mean percent of resorbed implants per litter was 34, 62, and 90 at 800, 1,200, and 1,800 mg/kg, respectively. Live fetuses showed dose-dependent reductions in weight and length. The mean frequency of soft tissue malformations ranged from 9% at the low dose to 97% at the high dose. These were principally in the cardiovascular system (interventricular septal defect, levocardia). Skeletal malformations were found only at 1,200 and 1,800 mg/kg and were mainly in the orbit. Based on these observations TCA was considered to be developmentally toxic in the pregnant rat at doses of 330 mg/kg and above.

Abnormalities, Drug-Induced↗

PubMed1990

Subchronic 90 day toxicity of dichloroacetic and trichloroacetic acid in rats.

Male Sprague-Dawley rats were treated with either dichloroacetic acid (DCA) or trichloroacetic acid (TCA) in the drinking water at levels of 0, 50, 500 and 5000 ppm for a period of 90 days to determine the toxicities associated with subchronic exposure. All animals were sacrificed and examined for gross and histopathologic lesions, serochemical changes, immune dysfunction, hepatic peroxisomal and mixed function oxidase enzyme induction and organ-body weight changes. Animals treated with DCA had decreased body weight gains (500 and 5000 ppm) and decreased total serum protein (all doses). Rats given either TCA (5000 ppm) or DCA (500 or 5000 ppm) had increased liver and kidney organ to body weight ratios. Rats offered DCA had significantly elevated alkaline phosphatase (500 and 5000 ppm) and alanine-amino transferase (5000 ppm). No consistent immunotoxicity was observed in animals exposed to either compound. Rats treated with 5000 ppm TCA or DCA had significantly increased hepatic peroxisomal beta-oxidation activity. These data, along with histopathologic changes, suggest that TCA and DCA produce substantial systemic organ toxicity to the liver and kidney during a 90-day subchronic exposure, although only at doses greater than those expected to occur in the environment.

Alanine Transaminase↗

PubMed1998

A human physiologically based pharmacokinetic model for trichloroethylene and its metabolites, trichloroacetic acid and free trichloroethanol.

Nine male and eight female healthy volunteers were exposed to 50 or 100 ppm trichloroethylene vapors for 4 h. Blood, urine, and exhaled breath samples were collected for development of a physiologically based pharmacokinetic (PBPK) model for trichloroethylene and its two major P450-mediated metabolites, trichloroacetic acid and free trichloroethanol. Blood and urine were analyzed for trichloroethylene, chloral hydrate, free trichloroethanol and trichloroethanol glucuronide, and trichloroacetic acid. Plasma was analyzed for dichloroacetic acid. Trichloroethylene was also measured in exhaled breath samples. Trichloroethylene, free trichloroethanol, and trichloroacetic acid were found in blood samples of all volunteers and only trace amounts of dichloroacetic acid (4-12 ppb) were found in plasma samples from a few volunteers. Trichloroethanol glucuronide and trichloroacetic acid were found in urine of all volunteers. No chloral hydrate was detected in the volunteers. Gender-specific PBPK models were developed with fitted urinary rate constant values for each individual trichloroethylene exposure to describe urinary excretion of trichloroethanol glucuronide and trichloroacetic acid. Individual urinary excretion rate constants were necessary to account for the variability in the measured cumulative amount of metabolites excreted in the urine. However, the average amount of trichloroacetic acid and trichloroethanol glucuronide excreted in urine for each gender was predicted using mean urinary excretion rate constant values for each sex. A four-compartment physiological flow model was used for the metabolites (lung, liver, kidney, and body) and a six-compartment physiological flow model was used for trichloroethylene (lung, liver, kidney, fat, and slowly and rapidly perfused tissues). Metabolic capacity (Vmaxc) for oxidation of trichloroethylene was estimated to be 4 mg/kg/h in males and 5 mg/kg/h in females. Metabolized trichloroethylene was assumed to be converted to either free trichloroethanol (90%) or trichloroacetic acid (10%). Free trichloroethanol was glucuronidated forming trichloroethanol glucuronide or converted to trichloroacetic acid via back conversion of trichloroethanol to chloral (trichloroacetaldehyde). Trichloroethanol glucuronide and trichloroacetic acid were then excreted in urine. Gender-related pharmacokinetic differences in the uptake and metabolism of trichloroethylene were minor, but apparent. In general, the PBPK models for the male and female volunteers provided adequate predictions of the uptake of trichloroethylene and distribution of trichloroethylene and its metabolites, trichloroacetic acid and free trichloroethanol. The PBPK models for males and females consistently overpredicted exhaled breath concentrations of trichloroethylene immediately following the TCE exposure for a 2- to 4-h period. Further research is needed to better understand the biological determinants responsible for the observed variability in urinary excretion of trichloroethanol glucuronide and trichloroacetic acid and the metabolic pathway resulting in formation of dichloroacetic acid.

Administration, Inhalation↗

PubMed1990

Development of a trichloroacetic acid precipitation assay for covalent adducts of thymidylate synthase.

The use of trichloroacetic acid as a protein precipitant and denaturant in the quantitative measurement of covalent complexes of thymidylate synthase is described. Enzyme inactivated with N[3H]ethylmaleimide and inhibitory ternary complex (formed with native enzyme, 5-[6-3H]fluoro-2'-deoxyuridylate, and methylenetetrahydrofolate) served as reagents which were used to establish the conditions under which trichloroacetic acid precipitation, washing, and solubilization steps provided quantitative results. The ternary complex formed by dihydrofolate reductase with [3H]methotrexate and NADPH was used as a control to assess whether tight, but noncovalent, enzyme:ligand complexes survived trichloroacetic acid precipitation. The fact that no counts above background were detected in the pellet of precipitated protein demonstrated that the noncovalent complexes were completely dissociated by this treatment. The dynamic range of linear response for the inhibitory ternary complex of thymidylate synthase spanned five orders of magnitude, and the assay detected levels of enzyme as low as 10 fmol, a value which was essentially limited by the specific radioactivity of 5-[6-3H]fluoro-2'-deoxyuridylate. The ability of the enzyme to bind 5-[6-3H]fluoro-2'-deoxyuridylate specifically, as measured by the trichloroacetic acid assay, generated a specific binding value of 13.4 nmol of enzyme/mg protein (assuming a binding ratio of 1.5 for the inhibitory ternary complex). Specific binding values were compared to specific activity values (obtained from the spectrophotometric assay) at each stage of purification of the enzyme from Lactobacillus casei and were found to give parallel results. The characteristics of the trichloracetic acid assay procedure, which exclusively detects covalent enzyme-ligand adducts, are compared to those for other ligand binding assays for thymidylate synthase.

Bacterial Proteins↗

PubMed1994

Standardizing chemical peel solution formulations to avoid mishaps. Great fluctuations in actual concentrations of trichloroacetic acid.

BACKGROUND: Chemical peeling using trichloroacetic acid (TCA) is a popular and long utilized procedure in dermatology and cosmetic surgery. OBJECTIVE: To determine the actual concentration of TCA in four disparate methods of preparation of solutions, expressed in the standard pharmaceutical method of weight to volume (wt/vol). METHODS: Method I was wt/vol, method II was weight to weight (wt/wt), method III was grams of TCA added to 100 cc water, and method IV was the usage of saturated TCA, and calling it 100%, then making appropriate dilutions. The amounts of TCA in each solution for methods II, III, and IV were converted, by calculation, to the wt/vol method. RESULTS: The relative concentrations of TCA, ranked by the wt/vol pharmaceutical standard, showed that from strongest to weakest: method IV > method II > method I > method III. CONCLUSIONS: Tremendous variations were found in the relative concentrations of TCA in these solutions. To avoid mishaps and complications, the wt/vol method should be used.

Chemexfoliation↗

PubMed1996

Obagi's modified trichloroacetic acid (TCA)-controlled variable-depth peel: a study of clinical signs correlating with histological findings.

Currently, no documentation correlates histological changes with clinical signs of depth of the trichloroacetic acid peel. Obagi identified clinical signs of depth of injury following topical trichloroacetic acid application, employing prepeel conditioning and a method for slowing trichloroacetic acid action. A three-part study of 20 patients was undertaken to determine whether Obagi's visual and palpatory signs of depth correlated histologically with depth of peel. Also analyzed were physiological mechanisms associated with these signs. Patients were pretreated and biopsy specimens were harvested before and after modified trichloroacetic acid peeling. The results largely confirmed the validity of Obagi's observations regarding the method of trichloroacetic acid peel described. These clinical signs are verified by histology and correlated with some findings by electron microscopy. Differentiation of papillary from upper reticular dermal penetration is particularly useful. Physiological explanations for the phenomena observed are proposed. The specificity and safety of peels may be improved with these criteria.

Acne Vulgaris↗

PubMed1990

Alpha 1-acid glycoprotein decreases recovery of total protein in urine when trichloroacetic acid is used to precipitate the proteins.

Total urine protein was measured in 132 samples by an automated benzethonium chloride method and the Ponceau-S/trichloroacetic acid (PS/TCA) method. Of these, 27% gave a result 0.1 g/L or more higher by the benzethonium chloride method. Of this 27%, most contained an abnormally high concentration of the acute-phase reactant, alpha 1-acid glycoprotein. By assaying urine containing added alpha 1-acid glycoprotein and albumin, we found that alpha 1-acid glycoprotein causes the PS/TCA method to underestimate the total urine protein concentration, whereas the benzethonium chloride method is unaffected. Not all urinary albumin was precipitated by TCA when alpha 1-acid glycoprotein was present. Therefore, protein methods in which trichloroacetic acid is used as a concentrating step before the assay will underestimate total urine protein when the concentration of alpha 1-acid glycoprotein is high.

Azo Compounds↗

PubMed1993

Treatment of photoaging. Facial chemical peeling (phenol and trichloroacetic acid) and dermabrasion.

A complete armamentarium using phenol, trichloroacetic acid, and dermabrasion allows the physician to successfully treat a variety of difficult photoaged skin problems in a consistent fashion. These three techniques have their specific indications, and patient selection is the key to a successful outcome. Proper attention to technical detail will allow the physician to fine-tune technique to meet the individual's needs. It is important to realize that phenol, trichloroacetic acid, and dermabrasion are not exclusive of each other, but are additive in their value. As one becomes well versed in these differing treatment modalities, one can tailor these techniques to obtain consistent results according to the needs and desires of the patient.

Chemexfoliation↗

PubMed1987

Protein kinase assay by paper-trichloroacetic acid method: high performance using phosphocellulose paper and washing an ensemble of samples on flat sheets.

Phosphocellulose paper has been found to be the paper of choice in assaying protein kinase activities using [gamma-32P]ATP by the trichloroacetic acid method of precipitation and washing. A study of binding of ATP of increasing concentrations at constant specific activity with Whatman 3MM or ATP-coated Whatman 3 MM papers (in vogue) versus phosphocellulose paper (proposed here) has shown that the latter has the least affinity for ATP when washing is done with either trichloracetic acid or trichloroacetic acid containing pyrophosphate. In an experiment where the placental cytosolic protein kinase was serially diluted, the phosphocellulose paper was found to give higher signal/noise ratios at all dilutions studied compared to the other two papers. With regard to the technological side of washing the papers, we have found that the traditional method of cutting papers into small squares before loading the samples is perhaps not the best. Instead, we propose the use of a flat sheet matrix for loading the samples because this method ensures uniformity of washing among the samples while shaking is performed on a simple shaker. In addition, the whole paper matrix can provide an almost instantaneous autoradiogram of hundreds of samples facilitating biochemical experimentation with protein kinases.

Adenosine Triphosphate↗

PubMed1990

Subacute toxicity of trichloroacetic acid in male and female rats.

Trichloroacetic acid, TCA, is a water chlorination by-product similar to dichloroacetic acid, DCA. Because DCA has been shown to have effects on intermediary metabolism, TCA was tested to determine if it possesses similar capabilities. The effects were more pronounced in females. High doses of TCA (2.45 mumol/kg three times) decreased plasma glucose and lactate concentrations and liver lactate concentration. DCA had similar, less pronounced effects. In males DCA and TCA each decreased plasma lactate concentrations. Rats were exposed to TCA in drinking water for 14 days. The highest concentration (2.38 g/l) caused decreases of water and food consumption and loss of body weight. At 7 days females had decreased urine volume accompanied by a modest increase of urine osmolality, resulting in a significant decrease of excretion of solute. Concentrations of glucose in plasma and lactate in tissues were not significantly affected by this subchronic TCA exposure. These results indicate that TCA may have effects on intermediary metabolism similar to those of DCA.

Animals↗

PubMed1995

Ras oncogene activation during hepatocarcinogenesis in B6C3F1 male mice by dichloroacetic and trichloroacetic acids.

Dichloroacetic (DCA) and trichloroacetic (TCA) acids, two major by-products formed during chlorine disinfection of drinking water, increase the incidence of tumors in B6C3F1 mice by 6- and 3-fold respectively. In order to understand better the mechanism by which these two compounds induce liver tumors, the incidence and spectrum of mutations in the K- and H-ras proto-oncogenes in these tumors were analyzed. DNA from spontaneous, DCA- and TCA-induced liver tumor from B6C3F1 male mice was evaluated for point mutations in exons 1, 2 and 3 of the two genes by single-stranded conformation polymorphism. Results demonstrated a similar incidence of mutations for exon 2 of H-ras in spontaneous carcinomas (58%), and in carcinomas induced by DCA 3.5 g/l (50%), 1.0 g/l (48%) and TCA 4.5 g/l (45%). Only four showed mutations in the other exons of Hras or in K-ras. Sequence analysis of spontaneous tumor samples with second exon H-ras mutations revealed a change in codon 61 from CAA to AAA in 80% and CAA to CGA in 20% of tumors. In contrast, tumors with H-ras mutations from DCA-treated mice revealed a H-61 change from CAA to AAA in 21% at 3.5 g/l and 16% at 1.0 g/l. CAA to CGA was observed in 50% of tumors from mice given DCA 3.5 or 1.0 g/l, and CAA to CTA was present in 29% and 34% of the two dosage groups respectively. Interestingly, TCA showed the same mutational spectrum as the spontaneous liver tumors. The data indicates that induction of liver carcinoma by DCA and TCA involves activation of the H-ras proto-oncogene at a frequency similar to that observed in spontaneous tumors. However, the mechanism(s) for including hepatocellular carcinoma does not appear to be identical for DCA and TCA.

Animals↗

PubMed1998

Histopathologic changes of the eyelid skin following trichloroacetic acid chemical peel.

The use of trichloroacetic acid (TCA) as a periorbital and eyelid peel for skin rejuvenation is gaining significant acceptance among oculoplastic surgeons, dermatologists, and other surgery groups. In spite of the current enthusiasm, there remain potentially serious complications resulting from any periorbital peel. Cases of cicatricial ectropion have been reported in phenol-peeled patients, and lower eyelid ectropion has reportedly occurred in patients undergoing deep eyelid peel in conjunction with a blepharoplasty (1,2). To avoid this complication, it is necessary to better understand the depth of the wound produced by different strengths and combinations of peeling agents applied to living eyelid tissue and, more important, to determine the concentrations of TCA that are likely to lead to cicatricial ectropion when applied in a consistent fashion. We chose upper-eyelid skin because it is easier to obtain for histopathologic study than lower-eyelid skin and, in our experience, is more sensitive to hypertrophic changes after chemical peeling or carbon dioxide laser resurfacing. We applied TCA to the preseptal skin of 10 patients 48 h before standard upper-eyelid blepharoplasty. The acid was applied to produce a "frost," using varying concentrations of acid, ranging from 20 to 50%. The treated skin removed at the time of blepharoplasty was reviewed in a masked fashion by a dermatopathologist to determine the depth of necrosis. We found that superficial peels with necrosis involving 30% of the epidermis were produced by the lowest-concentration combination of TCA applied (20% followed by 0%). As the strength increased, so did the depth of peel. The combination of 50% followed by a second application of 50% produced the deepest peel, with necrosis into the papillary dermis. This finding would indicate that the chance of developing cicatricial ectropion with any of the tested combinations of TCA should be very remote.

Administration, Topical↗

PubMed2003

Uptake, translocation and fate of trichloroacetic acid in a Norway spruce/soil system.

Trichloroacetic acid (TCA) is a secondary atmospheric pollutant formed by photooxidation of chlorinated solvents in the troposphere--it has, however, recently been ranked among natural organohalogens. Its herbicidal properties might be one of the factors adversely affecting forest health. TCA accumulates rapidly in conifer needles and influences the detoxification capacity in the trees. The aim of the investigations--a survey of which is briefly given here--was to elucidate the uptake, distribution and fate of TCA in Norway spruce. For this purpose young nursery-grown plants of Norway spruce (Picea abies (L.) Karst.) were exposed to [1,2-14C]TCA and the fate of the compound was followed in needles, wood, roots, soil and air with appropriate radio-indicator methods. As shown by radioactivity monitoring, the uptake of TCA from soil by roots proceeded most rapidly into current needles at the beginning of the TCA treatment and was redistributed at later dates so that TCA content in older needles increased. The only product of TCA metabolism/biodegradation found in the plant/soil-system was CO(2) (and corresponding assimilates). TCA biodegradation in soil depends on TCA concentration, soil humidity and other factors.

Air Pollutants↗

PubMed2006

Neuroembryopathic effect of trichloroacetic acid in rats exposed during organogenesis.

BACKGROUND: Halogenated hydrocarbons such as trichloroacetic acid (TCA) are among the most common water supply contaminants in the world. This study examines the effect of TCA on the developing brain of the Charles Foster rat. METHODS: Adult pregnant rats were placed in the test group and exposed to various concentration of TCA (i.e., 1000, 1200, 1400, 1600, and 1800 mg/kg body weight [b.w.]) by oral gavage throughout the period of organogenesis from Gestation Day (GD) 6-15 of gestation. Trichloroacetic acid was administered in the form of trichloroacetate, which is reduced to TCA in the body. The control mother rats were administered an equal volume of distilled water. Fetal brains were examined for their external and histological malformation. RESULTS: On GD 19, TCA administration led to an initial increase of brain weight at 1000 mg/kg b.w. and then a weight reduction after TCA doses of 1200 mg/kg b.w. and over. The brain of the formalin-fixed fetuses at 1000 and 1200 mg/kg b.w. showed hydrocephalus with breech of the ependymal lining, altered choroids plexus architecture, and increased apoptosis. At doses of 1400 mg/kg b.w. and above, the brain showed not only enhanced apoptosis of the neuronal cells, but extravasation of erythrocytes within the cortical parenchyma, vacuolation of the neuropil, and multiple cavity formation. CONCLUSION: With an increase in dose of TCA i.e., 1200 mg/kg b.w. and above, there is enhanced apoptosis, leading to increased neuronal death, which consequently led to the reduction in the brain weight as compared to controls. The fetal central nervous system is susceptible to the toxic effect of TCA.

Animals↗

PubMed1990

Single application treatment of human papillomavirus infection of the cervix and vagina with trichloroacetic acid: a randomized trial.

Treatment of human papillomavirus (HPV) infection of the lower genital tract with trichloroacetic acid was evaluated in a randomized, double-blind fashion at the Hospital of the University of Pennsylvania. Thirty-four patients who had colposcopic and histologic evidence of HPV without dysplasia were entered into the study and randomly placed into either a treatment or placebo group. The treatment group received a single topical application of 50% trichloroacetic acid to the vagina and cervix on day 1. The placebo group was treated in the same manner using saline. The patients were evaluated at 4 and 16 weeks post-treatment for cytologic and histologic evidence of HPV. No differences between the treatment and placebo groups were found. Only one of 16 patients in the treatment group and three of 18 in the placebo group were free of HPV infection at the 4- and 16-week evaluations. Our data suggest that treatment of subclinical HPV infection with trichloroacetic acid is ineffective at this concentration.

Adolescent↗

PubMed1997

Manual resurfacing and trichloroacetic acid for the treatment of patients with widespread actinic damage. Clinical and histologic observations.

BACKGROUND: A facial resurfacing regimen combining manual abrasion of the skin and 25% trichloroacetic acid has been reported to produce excellent results, but the histologic depth of injury produced by this technique has not been studied. OBJECTIVE: To describe our experience with this technique treating patients with extensive actinic damage and to determine the histologic depth of injury produced. METHOD: We treated 40 patients using manual resurfacing and trichloroacetic acid, primarily for widespread actinic keratoses. Resurfacing tools included silicone carbide sandpaper, drywall screen, electrocautery tip cleaners, abrasive pads, scalpel blades, and curettes. Four patients underwent sequential biopsies to evaluate the depth of wounding using this technique. RESULTS: Manual resurfacing combined with trichloroacetic acid consistently produced excellent cosmetic results and nearly complete eradication of actinic keratoses. Histologically, treated areas showed replacement of the dermal elastotic band by newly formed collagen, a significantly deeper level of wounding than the Jessner's/35% trichloroacetic acid peel. There was no evidence for foreign body granulomas clinically or histologically as a result of the abrasive materials. CONCLUSIONS: The deeper level of this peel explains the improved cosmetic outcome and greater eradication of actinic keratoses. This treatment is particularly well suited for patients with extensive photodamage and widespread actinic keratoses.

Aged↗

PubMed1986

[Determining trichloroacetic acid in the urine by the gas chromatography method].

It has been found that the method of determination of trichloroacetic acid in urine after Monster and Boersma due to high detectability and specificity may be used for determination of trichloroacetic acid (TCA) in urine particularly when aimed at evaluation of exposure to tetrachloroethylene (PERC) or to trichloroethylene (TRI) et low concentrations range. The improvement of determinations precision has been obtained by introduction of internal standard. In case of application of full procedure for trichloroacetic acid solutions in urine ranging from 1.0 to 15.0 mg/1, the relative standard deviation amounted to: sr = 0.063 (n = 21).

Air Pollutants, Occupational↗

PubMed1995

Analysis of trichloroacetic acid in the urine of workers occupationally exposed to trichloroethylene by capillary gas chromatography.

A gas chromatographic procedure is described for the determination of trichloroacetic acid in urine, the major metabolite of trichloroethylene exposure. Trichloroacetic acid was derivatised to its methyl ester with BF3/methanol reagent and then extracted into toluene and analysed by capillary gas chromatography using electron-capture detection. The response was linear in the range 0.4-100 mg/l of trichloroacetic acid in urine and showed a relative recovery of 99.6%. The procedure is suitable for monitoring occupational exposure to trichloroethylene.

Absorption↗