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EC number: 219-956-7
CAS number: 2582-30-1
In vitro tests:
Aminoguanidinium hydrogen carbonate was tested in the Ames test in
1982 (according to Ames et al. 1973 Proc nat Acac Sci (USA) 70,
2281-2285; Ames et al. 1975 Mutation Res 31, 347-364) using Samonella
typhimurium TA 98, TA 100, TA 1535, TA1537 in the presence and in the
absence of a metabolic activation system.
The applied concentrations are 0 (negative controls), 20,100, 500,
2500 and 12500 µg/plate. There were no indications of a mutagenic effect
of aminoguanidinium hydrogen carbonate up to the highest test dose.
In 1988, aminoguanidinium hydrogen carbonate was tested again in
the Ames test according to OECD TG 471 and GLP using preincubation
methodology using S. typhimurium TA 98, TA100, TA1535, TA 1537 in the
presence and in the absence of a metabolic activation system and
concentrations of the test item up to 14000 µg/plate.
Only S typhimurium TA 1535 showed mutagen activity in the absence
of the activation system from 8000 µg/plate onwards, thus in
concentrations which exceed the requirements of the guideline.
In a recently performed Ames test (JETOC 2000) aminoguanidinium
hydrogen carbonate was tested according to the OECD TG 471 and GLP using
Salmonella typhimurium TA98, TA100, TA1535, TA1537, and E. coli
WP2uvrA/pKM101 in the presence and absence of S9-mix and preincubation
methodology. The concentrations used ranged from 0 (solvent control) up
to 5000 µg/plate according to the requirement to the guideline.
Aminoguanidinium hydrogen carbonate did not show mutagenic
activity in any of the strains used. The positive controls were
mammalian cell gene mutation assay, mouse lymphoma L5178Y cells cultured
in vitro exposed to Aminoguanidinium hydrogen carbonate, at
concentrations of 43.75, 87.50, 175.00, 350.00, 700.00, 1400.00 µg/ml
for 4 hours with and without S9 -mix and 24 hours with S9 mix and
concentrations of 65.63, 131.25, 262.50, 525.00, 1050.00, 1400.00 µg/ml
with S9 mix for 4 hour exposure were not genotoxic under the conditions
of the test. The
positive controls induced the appropriate response. There was no
evidence of induced mutant colonies over background.
In vivo tests:
Four micronucleus are available.
Employing the micronucleus test according to OECD TG 474,
aminoguanidinium hydrogen carbonate was investigated in male and female
mice for a possible clastogenic effect on the chromosomes of bone marrow
erythroblasts. 24, 48 or 72 hours after the single oral application by
gavage of 0 or 7500 mg/kg bw, the animals were sacrificed.
An additional group of 20 females received a single dose of 5000
The animals treated with aminoguanidinium hydrogen carbonate
showed lasting symptoms of toxicity after the administration and in all
treatment groups animals died indicating that the MTD was exceeded in
The ratio of polychromatic to normochromatic erythrocytes was
altered, but not to a statistically significant degree. No indication of
a clastogenic effect was observed in any group or gender. However, in
the 72 hour interval, the males showed an increased ratio of
polychromatic erythrocytes with micronuclei. This increase, however, was
not statistically significant.
In a second micronucleus test aminoguanidinium hydrogen carbonate
was investigated in male mice for a possible clastogenic effect on the
chromosomes of bone marrow erythroblasts.
72 hours after the single oral application by gavage of 0, 5000,
6000, 7000 mg/kg bw the animals were sacrificed. The animals treated
with aminoguanidinium hydrogen carbonate showed lasting symptoms of
toxicity after the administration. In all treatment groups animals died,
indicating that the MTD was exceeded in this test.
In contrast to the first experiment the ratio of polychromatic to
normochromatic erythrocytes was not altered. Due to the high level of
acute toxicity seen in this study slight clastogenic effects observed at
doses with high mortality were attributed to cytotoxicity rather than to
In a third micronucleus test aminoguanidinium hydrogen carbonate
was investigated in female mice for a possible clastogenic effect on the
chromosomes of bone marrow erythroblasts.
72 hours after the single oral application by gavage of 0, 500,
1000, 2000 mg/kg bw the animals were sacrificed.
The 500 mg/kg group tolerated the treatment without any symptoms.
From 1000 mg/kg bw onwards animals showed apathy and suffered from
diarrhoe.3 animals of the high dose group died. The ratio of
polychromatic to normochromatic erythrocytes was not altered. No
indication of a clastogenic effect of aminoguanidinium hydrogen
carbonate was found after a single treatment with up to 2000 mg/kg. The
ratio of polychromatic to normochromatic erythrocytes was not altered.
An unscheduled DNA Synthesis (UDS) Assay was employed to
investigate aminoguanidinium hydrogen carbonate in vivo in male rats for
a possible genotoxic effect on the DNA of liver cells.
Animals received aminoguanidinium hydrogen carbonate in a single
oral dose of 1000 mg/kg and 2500 mg/kg, respectively.
The males treated with aminoguanidinium hydrogen carbonate showed
symptoms of toxicity after administration, starting at 1000 mg/kg. 1 of
5 animals died before the end of the test due to the acute oral toxicity
of aminoguanidinium hydrogen carbonate at a dose of 2500 mg/kg.
The liver cells of groups treated with aminoguanidinium hydrogen
carbonate and of the negative controls were prepared 4 and 16 hours
after administration No cytotoxicity was observed in isolated
hepatocytes of exposed animals.
No indications of UDS-induction by Aminoguanidinium hydrogen
carbonate were found after a single oral treatment with 1000 mg/kg and
Aminoguanidinium hydrogen carbonate is not considered to be
mutagenic or clastogenic.
Based on the available data no classification or labelling is
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