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EC number: 231-901-9
CAS number: 7778-39-4
an in vitro gene mutation study, bacterial and mammalian cells were
exposed to sodium arsenite in a series of tests:
cell gene mutation assays:
Spot test (WP2, WP6, WP10 and WP44s-NF): 0.01 and 0.1 M
Treat and plate protocol (WP2 and WP6): 25 mM
Fluctuation tests (WP2): Experiment 1 (0.4 mM) and Experiment 2 (1 and 2
Induction of λ prophage: WP2s (λ): Experiment 1 (10 mM, 20 minutes) and
Experiment 2 (1 and 10 mM, 30 minutes)
hamster lung fibroblasts (V79):
Ouabain resistant marker: 0.5 µM, 2 days and 5.0 µM, 1 hour
Thioguanine resistant marker: 20 and 100 µM, 1.5 hours
the E. coli system, Trp+ revertants were not induced by arsenite in spot
tests, treat and plate protocols, or fluctuation tests. The mutator
effect of a tif-1 strain was partially blocked by arsenite. Arsenite did
not cause the induction of lambda prophage. In Chinese hamster cells,
arsenite did not induce ouabain-resistant mutants or
the test conditions, sodium arsenite is not considered as mutagenic to
E. coli or to Chinese hamster cells.
In an in vitro mammalian cell gene mutation
test performed similarly to OECD guideline 476, L5178Y/ TK+/- mouse
lymphoma cells were exposed to sodium arsenate at concentrations of 26,
34, 46, 61 and 81 μg/mL in the absence of metabolic activation and the
exposure duration was 3 hours.
Positive controls (methyl methane
sulphonate) induced the appropriate response. No significant increases
in mutant frequency were observed following treatment of sodium arsenate
in the absence of metabolic activation.
Under the test conditions, sodium arsenate
is not considered as mutagenic in mouse lymphoma L5178Y cells.
In an in vitro chromosomal aberration assay
conducted similarly to OECD Guideline 473, whole blood cultures were
incubated for 72 hours and treated with various concentrations (1-10-10
µM) of sodium arsenite for the last 24 hours. Also, mitotic arrest was
evaluated in cultures treated for the last 2 hours. Cells were harvested
and samples were processed for evaluation of aneuploidogenic and mitotic
arrest. Number of chromosomes in 200 metaphases of first and second
division cells was scored.
Positive controls (colcemid at 10-2 µM)
induced the appropriate response. A dose-related effect was observed:
highest concentration (10-2 µM sodium arsenite) induces 28.33 and 22.4%
hyperploid cells in first and second division respectively and 29%
tetraploid cells. Sodium arsenite produced 40.24 and 12.93% of the
mitotic arrestant effect at 10-2 µM and 10-10 µM, respectively). A
different individual susceptibility effect was observed in both
parameters and confirmed with the chromosome aberrations levels induced
by arsenic in the same donors.
Under the test conditions, sodium arsenite
was found to have an aneuploidogenic and a mitotic arrestant effect in
cultured human lymphocytes. The authors of the report did not include a
comment in their summary of the report, but a positive effect was also
observed in terms of an increase in chromosome aberrations.
An in vitro gene mutation assay was
conducted with sodium arsenite in the supF gene of pZ189 shuttle vector
system in DNA repair proficient GM0637 human fibroblasts to determine
whether arsenic alone induces mutation and whether the combination of
arsenic and UV irradiation leads to a yield of mutants greater than the
sum of the arsenic or UV treatments alone. Sodium arsenite was tested at
the concentrations of 1, 2.5 and 5.0 µM in GM 637 human fibroblasts for
72 hours and plasmid was irradiated with 320 J/m2. Poisson distribution
followed by student’s t-test was used to assess the effects of sodium
arsenite on mutant frequencies.
Sodium arsenite alone produced significant
increases in the pZ189 mutant frequency at the concentration of 5.0 µM,
whereas 1 and 2.5 µM arsenite were not mutagenic. UV irradiation (320
J/m2) increased the yield of mutants 3.5-fold above the background rate.
When UV-irradiated plasmid was allowed to replicate in fibroblasts
treated with sodium arsenite, the yields of mutations were significantly
greater (p < 0.01) than the yield expected and the greatest potentiation
of UV-induced mutations (4.9-fold) was observed at 1 µM arsenite.
Restriction digest and DNA sequencing analyses indicated that arsenite
alone produces large-scale rearrangements, frameshifts and base
substitutions. Hotspots for deletions were observed to be associated
with a previously reported deletion hotspot involving 5'-CpC and runs of
cytosines. Base substitutions observed involved A:T→T:A transversions.
Under the test conditions, arsenite alone
was found to be mutagenic in human fibroblast cells and potentiated the
UV-induced mutations in plasmid DNA.
Not to be classified because no positive results have been reported in
the in vivo study.
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