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EC number: 200-927-2
CAS number: 76-03-9
Trichloroacetic acid has been tested for in vitro genotoxicity in a
series of Ames tests, DNA damage and/or repair assays and point mutation
assay in Aspergillus nidulans. In all these studies, trichloroacetic
acid gave negative results, except in one, in which dimethyl sulfoxide
(DMSO) was used as a solubiliser. The evidence supports the hypothesis
that a reaction between trichloroacetic acid and DMSO produces a
short-lived intermediate product(s) that could be responsible of the
time-limited mutagenicity found to be induced by this solution.
Two in vitro cytogenetic assays in human lymphocytes were conducted with
trichloroacetic acid. In the first, trichloroacetic acid, as free acid,
was added to whole blood cultures in the presence and absence of an
auxiliary metabolic activation system (rat liver S9-mix). In the second
assay, neutralised trichloroacetic acid was tested also in the presence
and absence of S9-mix. Dose-related statistically significant increases
in the incidence of chromosomal aberrations, associated with significant
reductions in the pH of the cultures treated with trichloroacetic acid
were observed. Treatment with neutralised trichloroacetic acid did not
result in the induction of chromosomal aberrations. The authors
concluded from the results of these two in vitro cytogenetic assays that
trichloroacetic acid shows no intrinsic potential to induce cytogenetic
damage in the human lymphocyte chromosomal aberration assay when tested
up to cytotoxic concentrations.
An in vitro gene mutation assay (method similar to OECD guideline 476)
was performed. Trichloroacetic acid was mutagenic only in the presence
of S9 activation in L5178Y/TK+/- -3.7.2c mouse lymphoma cells. The
authors noted that trichloroacetic acid was the least potent mutagens
that they had evaluated.
In-vivo tests were conducted on chromosomal aberrations, DNA strand
breaks, oxidative DNA damage and DNA synthesis. An in vivo well
conducted bone marrow micronucleus study in mice reported negative
results (Mackay et al. 1995). In contrast, statistically significant
(but non-dose related) increases in the frequency of cells containing
micronuclei were observed in the Bhunya and Behera study (1987). Mackay
et al. proposed that the positive results previously observed with
trichloroacetic acid may have been due to a non-genotoxic mechanism,
possible caused by physicochemically induced stress, resulting from
intraperitoneal pH changes.
Based on the discussion presented above, it is considered that the
available evidence does not suggest that trichloroacetic acid is a
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