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Trichloroacetic acid (TCA) (Final, 2011)


  • 1.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    A physiologically based pharmacokinetic model for trichloroethylene and its metabolites, chloral hydrate, trichloroacetate, dichloroacetate, trichloroethanol, and trichloroethanol glucuronide in B6C3F1 mice

    Authors: Abbas, R; Fisher, JW
    (1997) Toxicology and Applied Pharmacology 147:15-30.
    Minus Sign. Click to see only selected choices. A six-compartment physiologically based pharmacokinetic (PBPK) model for the B6C3F1 mouse was developed . . . Plus Sign. Click to expand choices. A six-compartment physiologically based pharmacokinetic (PBPK) model for the B6C3F1 mouse was developed for trichloroethylene (TCE) and was linked with five metabolite submodels consisting of four compartments each. The PBPK model for TCE and the metabolite submodels described oral uptake and metabolism of TCE to chloral hydrate (CH). CH was further metabolized to trichloroethanol (TCOH) and trichloroacetic acid (TCA). TCA was excreted in urine and, to a lesser degree, metabolized to dichloroacetic acid (DCA). DCA was further metabolized. The majority of TCOH was glucuronidated (TCOG) and excreted in the urine and feces. TCOH was also excreted in urine or converted back to CH. Partition coefficient (PC) values for TCE were determined by vial equilibrium, and PC values for nonvolatile metabolites were determined by centrifugation. The largest PC values for TCE were the fat/blood (36.4) and the blood/air (15.9) values. Tissue/blood PC values for the water-soluble metabolites were low, with all PC values under 2.0. Mice were given bolus oral doses of 300, 600, 1200, and 2000 mg/kg TCE dissolved in corn oil. At various time points, mice were sacrificed, and blood, liver, lung, fat, and urine were collected and assayed for TCE and metabolites. The 1200 mg/kg dose group was used to calibrate the PBPK model for TCE and its metabolites. Urinary excretion rate constant values were 0. 06/hr/kg for CH, 1.14/hr/kg for TCOH, 32.8/hr/kg for TCOG, and 1. 55/hr/kg for TCA. A fecal excretion rate constant value for TCOG was 4.61/hr/kg. For oral bolus dosing of TCE with 300, 600, and 2000 mg/kg, model predictions of TCE and several metabolites were in general agreement with observations. This PBPK model for TCE and metabolites is the most comprehensive PBPK model constructed for P450-mediated metabolism of TCE in the B6C3F1 mouse. Copyright 1997 Academic Press.
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  • 2.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    Administration of subtoxic doses of t-butyl alcohol and trichloroacetic acid to male Wistar rats to study the interactive toxicity

    Authors: Acharya, S; Mehta, K; Rodrigues, S; Pereira, J; Krishnan, S; Rao, CV
    (1995) Toxicology Letters 80:97-104.
    Minus Sign. Click to see only selected choices. Tertiary butyl alcohol and trichloroacetic acid (TCA) are known to be contaminants in drinking water. . . . Plus Sign. Click to expand choices. Tertiary butyl alcohol and trichloroacetic acid (TCA) are known to be contaminants in drinking water. In order to evaluate the interactive toxicity of t-butyl alcohol (TBA) with TCA, young male Wistar rats were dosed through water at a dose level of TBA (0.5% v/v), 25 ppm TCA 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. There was remarkable loss of body weight and significantly decreased liver triglycerides in the treatment groups in the order of TBA+TCA, TCA, TBA and increased liver weights were observed. Serum succinate dehydrogenase (SDH) levels were significantly increased in TCA- and TBA+TCA-treated groups. There was no significant change in serum alanine (GPT), aspartate (GOT) aminotransferase, serum alkaline (ALP) and acid (ACP) phosphatase levels as well as liver glutathione (GSH) and liver and serum cholesterol levels in the treated groups. But serum triglycerides, liver glycogen, serum glucose (only in TBA- and TCA-treated animals) were significantly high in the treated groups. Lipid peroxidation measured by diene conjugation was significant in TBA+TCA-treated group and kidney GSH levels were significantly low in the treated groups. These results show that interaction of TBA+TCA does bring about alteration in biochemical parameters which may play a pivotal role in toxic responses on long-term exposure.
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  • 3.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    A histopathological study of liver and kidney in male Wistar rats treated with subtoxic doses of t-butyl alcohol and trichloroacetic acid

    Authors: Acharya, S; Mehta, K; Rodriguez, S; Pereira, J; Krishnan, S; Rao, CV
    (1997) Experimental and Toxicologic Pathology 49:369-373.
    Minus Sign. Click to see only selected choices. Tertiary butyl alcohol and trichloroacetic acid are known to be contaminants in drinking water. In order . . . Plus Sign. Click to expand choices. 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.
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  • 4.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    Pharmacokinetic modeling of trichloroethylene and trichloroacetic acid in humans

    Authors: Allen, BC; Fisher, JW
    (1993) Risk Analysis 13:71-86.
    Minus Sign. Click to see only selected choices. The development and application of appropriate physiologically based pharmacokinetic (PBPK) models of . . . Plus Sign. Click to expand choices. The development and application of appropriate physiologically based pharmacokinetic (PBPK) models of chemical contaminants will provide a rational basis for risk assessment extrapolation. Trichloroethylene (TCE) is a widespread contaminant found in soil, groundwater, and the atmosphere. Exposures to TCE and its metabolites have been found to be carcinogenic in rodents. In this study, a PBPK model for TCE and its major metabolite, trichloroacetic acid (TCA), is developed for humans. The model parameters, estimated from the relevant published literature on human exposures to TCE and its metabolites, are described. Key parameters describing the metabolism of TCE and the kinetics of TCA were estimated by optimization. The optimization was accomplished by simultaneously matching model predictions to observations of TCE concentrations in blood and exhaled breath, TCA plasma concentrations, and urinary TCA excretion from five published studies. The optimized human PBPK model provides an excellent description of TCE and TCA kinetics. The predictions were especially good for TCA plasma concentrations following repeated TCE inhalation, an exposure scenario similar to that occurring in the workplace. The human PBPK model can be used to estimate dose metrics resulting from TCE exposures and is therefore useful when considering the estimation of human health risks associated with such exposures.
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  • 5.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    Medium-depth chemical peels in the treatment of acne scars in dark-skinned individuals

    Authors: Al-Waiz, MM; Al-Sharqi, AI
    (2002) Dermatologic Surgery 28:383-387.
    Minus Sign. Click to see only selected choices. Multiple modalities are available for treating acne scars, one of which is chemical peeling.

    Plus Sign. Click to expand choices. Multiple modalities are available for treating acne scars, one of which is chemical peeling.

    To evaluate the efficacy of medium-depth peels in the treatment of acne scars.

    A total of 15 patients (14 women and 1 man) were seen between November 1998 and March 2000. A medium-depth chemical peel was performed. The peel was performed using a combination of Jessner's solution followed by the application of 35% trichloroacetic acid (TCA). The mean age of patients who entered the study was 28 years. A total of 42 peeling sessions were performed: 13 patients had the full three-session regiment, 1 patient had two sessions, and 1 had only one session.

    Patients in our study had two forms of acne scars, the atrophic saucer or crater-like form and the pitted (ice-pick) form. Improvement occurred in all except one of our patients. Significant improvement (greater than 75% clearance of lesions) occurred in 1 patient (6.6%), moderate improvement (51-75% clearance) in 8 patients (53.3%), mild improvement (26-50% clearance) in 4 patients (26.6%), minimal improvement (1-25% clearance) in 1 patient (6.6%), and no response in 1 patient (6.6%). All patients had different combinations of the above two forms. Four patients (26.6%) had mainly pitted scars and deep atrophic scars. The clinical response in those patients was moderate, mild, minimal, and no response, respectively. The remainder of our patients had mainly atrophic scars of moderate depth. Nine patients (73.4%) suffered from transient postinflammatory hyperpigmentation. In two of them it was preceded by erythema that lasted for more than 1 month. All patients were free of noticeable pigmentation 3 months after the final peel. Patients in whom hyperpigmentation did not develop were of light brown complexion.

    We conclude that medium-depth chemical peel is a safe and effective method of treating acne scars even in patients with dark complexion.
  • 6.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
    Peer
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    Nuclear hormone receptors and gene expression

    Authors: Aranda, A; Pascual, A
    (2001) Physiological Reviews 81:1269-1304. [Review]
    Minus Sign. Click to see only selected choices. The nuclear hormone receptor superfamily includes receptors for thyroid and steroid hormones, retinoids . . . Plus Sign. Click to expand choices. The nuclear hormone receptor superfamily includes receptors for thyroid and steroid hormones, retinoids and vitamin D, as well as different "orphan" receptors of unknown ligand. Ligands for some of these receptors have been recently identified, showing that products of lipid metabolism such as fatty acids, prostaglandins, or cholesterol derivatives can regulate gene expression by binding to nuclear receptors. Nuclear receptors act as ligand-inducible transcription factors by directly interacting as monomers, homodimers, or heterodimers with the retinoid X receptor with DNA response elements of target genes, as well as by "cross-talking" to other signaling pathways. The effects of nuclear receptors on transcription are mediated through recruitment of coregulators. A subset of receptors binds corepressor factors and actively represses target gene expression in the absence of ligand. Corepressors are found within multicomponent complexes that contain histone deacetylase activity. Deacetylation leads to chromatin compactation and transcriptional repression. Upon ligand binding, the receptors undergo a conformational change that allows the recruitment of multiple coactivator complexes. Some of these proteins are chromatin remodeling factors or possess histone acetylase activity, whereas others may interact directly with the basic transcriptional machinery. Recruitment of coactivator complexes to the target promoter causes chromatin decompactation and transcriptional activation. The characterization of corepressor and coactivator complexes, in concert with the identification of the specific interaction motifs in the receptors, has demonstrated the existence of a general molecular mechanism by which different receptors elicit their transcriptional responses in target genes.
  • 7.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    Modification of lipoperoxidative effects of dichloroacetate and trichloroacetate is associated with peroxisome proliferation

    Authors: Austin, EW; Okita, JR; Okita, RT; Larson, JL; Bull, RJ
    (1995) Toxicology 97:59-69.
    Minus Sign. Click to see only selected choices. Pretreatment of male B6C3F1 mice with clofibric acid (CFA) or trichloroacetic acid (TCA) in the drinking . . . Plus Sign. Click to expand choices. Pretreatment of male B6C3F1 mice with clofibric acid (CFA) or trichloroacetic acid (TCA) in the drinking water results in a marked decrease in the lipoperoxidative response as measured by the production of thiobarbituric acid reactive substances (TBARS) in mouse liver homogenates following acute dosing with TCA or dichloroacetic acid (DCA). Pretreatment with TCA or CFA also increased palmitoyl-CoA oxidase activity, microsomal 12-(ω) hydroxylation of lauric acid and expression of P450 4A isoforms. At the doses utilized, DCA-pretreatment did not increase the level of P450 4A protein, or markers of peroxisome proliferation. However, DCA-pretreatment did result in enhanced levels of TBARS, following acute dosing with DCA, compared to controls. Pretreatment with DCA, TCA, or CFA did not alter p-nitrophenol hydroxylation (an assay specific for P450 2E1), and no increases in immunodetectable P450 2E1, 4A, 1A1/2, 2B1/2 or 3A1 protein were observed. Assays from CFA- and TCA-pretreated mice suggest that the reduction in the TBARS response seen in TCA-pretreated animals results from activities associated with peroxisome proliferation. This might result from the induction of systems efficient in scavenging of peroxide intermediates or detoxification of aldehyde by-products of lipid peroxidation.
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  • 8.
    The "refereed" or "peer review" status of a journal comes from the Ulrichsweb Global Serials Directory (http://ulrichsweb.serialssolutions.com/), as supplied by the publisher. The term refers to the system of critical evaluation of manuscripts/articles by professional colleagues or peers. The content of refereed publications is sanctioned, vetted, or otherwise approved by a peer-review or editorial board. The peer-review and evaluation system is utilized to protect, maintain, and raise the quality of scholarly material published in serials. Publications subject to the referee process are assumed, then, to contain higher quality content than those that are not.
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    Lipid peroxidation and formation of 8-hydroxydeoxyguanosine from acute doses of halogenated acetic acids

    Authors: Austin, EW; Parrish, JM; Kinder, DH; Bull, RJ
    (1996) Fundamental and Applied Toxicology 31:77-82.
    Minus Sign. Click to see only selected choices. Chlorinated, brominated, and mixed bromochloro acetates are major by-products of water disinfection . . . Plus Sign. Click to expand choices. Chlorinated, brominated, and mixed bromochloro acetates are major by-products of water disinfection by chlorine or ozone. The chlorinated acetates, trichloroacetate (TCA) and dichioroacetate (DCA), are carcinogenic in rodents. Brominated analogs of TCA and DCA have received little study. TCA and DCA induce lipid peroxidation in the livers of rodents when administered acutely. Oxidative stress can also result in oxidative damage to DNA, most commonly measured as increases in 8-hydroxydeoxyguanosine (8-OHdG) adducts. In this study, the ability of acute doses of TCA, DCA, dibromoacetate (DBA), bromodichloroacetate (BDCA), and bromochloroacetate (BCA) to induce lipid peroxidation and 8-OHdG formation was examined. Male B6C3F1 mice developed significant increases in 8-OHdG/dG ratios in nuclear DNA isolated from livers when treated with haloacetates. The extent of 8-OHdG formation appeared to be related to the ability to induce thiobarbituric acid-reactive substances (TBARS). The order of potency was DBA = BCA > BDCA > DCA > TCA. The induction of 8-OHdG was found to be generally more sensitive to treatment with haloacetates than the TBARS response. Significantly elevated levels of 8-OHdG were observed at doses of DBA, BCA, and BDCA as low as 30 mg/kg. We suggest that formation of 8-OHdG by brominated haloacetates may contribute to their toxicological effects.
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  • 9.
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    Pathogenesis of hepatocellular carcinoma: Sequential cellular, molecular, and metabolic changes

    Author: Bannasch, P
    (1996) Progress in Liver Diseases 14:161-197. [Review]
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  • 10.
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    Significance of hepatic preneoplasia for cancer chemoprevention

    Authors: Bannasch, P; Nehrbass, D; Kopp-Schneider, A
    (2001) In Miller, AB; Bartsch, H; Bofetta, P; Dragsted, L; Vainio, H (Eds.), Biomarkers in cancer chemoprevention (pp. 223-240). Lyon, France: International Agency for Research on Cancer. [Review]
    Minus Sign. Click to see only selected choices. Hepatic preneoplasia represents an early stage in neoplastic development, preceding both benign and . . . Plus Sign. Click to expand choices. Hepatic preneoplasia represents an early stage in neoplastic development, preceding both benign and malignant neoplasia. This applies particularly to foci of altered hepatocytes (FAH), that precede the manifestation of hepatocellular adenomas and carcinomas in all species investigated. Morphological, microbiochemical and molecular biological approaches in situ have provided evidence for striking similarities in specific changes of the cellular phenotype of preneoplastic FAH emerging in experimental and human hepatocarcinogenesis, irrespective of whether this was elicited by chemicals, hormones, radiation, viruses or, in animal models, by transgenic oncogenes or Helicobacter hepaticus. Different types of FAH have been distinguished and related to three main preneoplastic hepatocellular lineages: (1) the glycogenotic-basophilic cell lineage, (2) its xenomorphic-tigroid cell variant, and (3) the amphophilic-basophilic cell lineage. The predominant glycogenotic-basophilic and tigroid cell lineages develop especially after exposure to DNA-reactive chemicals, radiation, hepadnaviridae, transgenic oncogenes and local hyperinsulinism, their phenotype indicating initiation by insulin or insulinomimetic effects of the oncogenic agents. In contrast, the amphophilic cell lineage of hepatocarcinogenesis has been observed mainly after exposure of rodents to peroxisome proliferators that are not directly DNA-reactive or to hepadnaviridae, the biochemical pattern mimicking an effect of thyroid hormone, including mitochondrial proliferation and activation of mitochondrial enzymes. Hepatic preneoplastic lesions are increasingly used as end-points in carcinogenicity testing, particularly in medium-term carcinogenesis bioassays. This has been complemented more recently by the use of FAH as indicators of chemoprevention, although possible pitfalls of this approach have to be considered carefully. Our ever-increasing knowledge on the metabolic and molecular changes that characterize preneoplastic lesions and their progression to neoplasia provides a new basis for rational approaches to chemoprevention by drugs, hormones or components of the diet.
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