Trichloroacetic acid toxicity

Sodium trichloroacetate [650-51-17, C2Cl202Na, is used as a herbicide for various grasses and cattails (2). The free acid has been used as an astringent, antiseptic, and polymerisation catalyst. The esters have antimicrobial activity. The oral toxicity of sodium trichloroacetate is quite low (LD q rats, 5.0 g/kg). Although very corrosive to skin, trichloroacetic acid does not have the skin absorption toxicity found with chloroacetic acid (28). 

Blossom, S.J., Pumford, N.R., and Gilbert, K.M., Activation and attenuation of apoptosis of CD4+ T cells following in vivo exposure to two common environmental toxicants, trichloroacetaldehyde hydrate and trichloroacetic acid, J. Autoimmun., 23, 211, 2004. 

Davis ME. 1992. Dichloroacetic acid and trichloroacetic acid increase ehloroform toxicity. J Toxicol Environ Health 37(1) 139-148. 

Mather GG, Exon JH, Roller LD Subchronic 90 day toxicity of dichloroacetic and trichloroacetic acid in rats. Toxicology 64 71-80, 1990... 

Two aliphatic acids possess, for grasses, many of the growth-distortion and toxicity effects associated with the synthetic auxins on dicotyledonous plants. Trichloroacetic acid and 2,2-dichloropropionic acid (dalapon), as the sodium salts, have been called grass "hormones or auxins, although Wilkinson184 could find no growth stimulation at low concentrations, and described dalapon as an antiauxin from its interference with indole-3-acetic acid effects. The herbicidal properties of trichloroacetate do not depend on its protein-denaturing ability, and those of 2,2-dichloropropionic acid involve, at least indirectly, the synthesis of pantothenic acid. 

These drugs include alcohols (ethchlorvynol, chloral hydrate), piperidinediones (glutethimide, methyprylon), and carbamates (meprobamate). They are rarely used in therapy, though the low cost of chloral hydrate makes it attractive for institutional use. Little is known about their molecular mechanisms of action. Most of these drugs are biotransformed to more water-soluble compounds by hepatic enzymes. Trichloroethanol is the pharmacologically active metabolite of chloral hydrate and has a half-life of 6-10 hours. However, its toxic metabolite, trichloroacetic acid, is cleared very slowly and can accumulate with the nightly administration of chloral hydrate. 

Inhalation of PCE is followed by prolonged urinary excretion of metabolites, primarily TCA. At more than 10 mg/1 of urinary TCA, workers may show some signs of toxicity. The finding of both di- and trichloroacetic acids in human urine following exposure to PCE has led to the suggestion of an oxirane as the metabolic intermediate (ref. 67b). 

Chloroform, dichloroacetic acid, and trichloroacetic acid are disinfection byproducts of water chlorination. In a study of laboratory rats it was shown that both dichloroacetic acid and trichloroacetic acid increase the renal toxicity of chloroform in test animals J10l... 

Trichloroacetic acid general information, toxicity, formulations and histology... 

Trichloroacetic acid (Figure 12.5), also known as trichloroethanoic acid and trichloromethane carboxylic acid, comes in the form of colorless or white crystals and has a distinctive sharp, pungent odor. As far as its toxicity is... 

Ayres achieved a medium-depth peel by combining phenol and trichloroacetic acid (TCA). These two formulas are no longer used today, as there are many other modern peel solutions that provide effective medium-depth peels using other molecules, such as TCA, that are not potentially toxic. 

Another study compared the toxicity of trichloroacetic acid (TGA) and phenol (Baker s solution) the conclusion was that it would appear advisable to set up a cardiac monitor during a ftill-face peel with Baker s solution, whereas TGA does not cause any type of arrhythmia. 

Attention has been directed in Chapter 2, Section 2.5 and Chapter 4, Section 4.1.2 to the occurrence of trichloroacetic acid in rainwater and its plausible production from the photolysis of chloroalkenes. A comparable issue in the formation of trifluoracetic add (TFA) and this has prompted a study of its sorption to and retention in soils. Although many soils did not retain TFA, retention was observed in those with a high organic content or with high concentrations of Fe and Al (Richey et al. 1997). In view of the extreme toxicity of TFA and its probably recalcitrance to microbial and chemical degradation, this is a disturbing issue. 

Protein synthesis was determined in the non-infected cells used as control and the HSV-1 and/or VSV infected cells, in order to obtain quantitative data on the toxicity and antiviral activity of the compounds assayed. Thus, 0.5 free medium methionine and 1 pCi/ml of methinione 32S were added to die cells and incubated at 37°C for 1 h. Thereafter the medium was siphoned off and the cells were washed with saline phosphate buffer and precipitated with 5% trichloroacetic acid (TCA). After 5 min, the acid was eliminated and the cells were washed twice with 96% ethanol,dried under an infrared light and dissolved in NaOH 0.1N with DSS. A liquid scintillation counter was used for the recount. The results showed no antiviral activity for die dihydro-f -agarofuran sesquiterpenes. 

Chloral hydrate is metabolized into two major metabolites—one which is pharmacologically active and relatively non-toxic (trichloroethanol) and the other which is toxic (trichloroacetic acid). Trichloroethanol is cleared fairly rapidly, with a half-life of less than ten hours. Trichloroacetic acid is cleared much more slowly, and will accumulate with nightly administration. 

The symptoms of poisoning from oral intake of trichloroethylene are nausea, vomiting, diarrhea, and gastric disturbances. The acute oral toxicity, however, is low. The oral LD50 value in mice is in the range 2500 mg/kg. Trichloroethylene metabolizes to trichloroacetic acid, which is excreted in the urine. 

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