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EC number: 215-252-9
CAS number: 1315-01-1
following in vitro tests for genetic toxicity have been performed on Tin
disulfide with a negative result:
test, Chromosomal Aberration test and gene mutation assay in mammalian
ovary (CHO) cells).
These results were confirmed by in vitro studies and an in vivo study on
the read-across substance tin sulfide.
genotoxic potential of the read-across test item Tin sulfide (CAS
1314-95-0) was also demonstrated
be negative in an Ames test, a Chromosomal Aberration test and a
Micronucleus test (in vivo).
following in vivo tests for genetic toxicity have been performed on
read-across substance tin
1314-95-0) with a negative result: Micronucleus
key bacterial reverse mutation assay was performed with a suspension of
Tin disulfide using TA98, TA100, TA1535 and TA1537 strains of S.
typhimurium and WP2uvrA E. coli with and without metabolic activation
(S9 fraction) prepared from Aroclor 1254 induced rat liver (Suresh,
2012). In a preliminary toxicity test, no cytotoxicity was seen up to
5000 µg/plate, with slight precipitation on the basal agar plates at
5000 µg/plate both with and without S9. Test doses were 50, 158, 500,
1580 and 5000 µg/plate using direct plate incorporation in the initial
mutation assay and 100, 266, 707, 1880 and 5000 µg/plate using
pre-incubation in the confirmatory assay. The results from the initial
as well as from the confirmatory assays, indicate the tested doses
showed no positive mutagenic increase in the mean numbers of revertant
colonies for all tester strains when compared to the respective vehicle
control plates, either with and without S9 up to the highest tested dose
of 5000 µg/plate. A supporting study with read-across substance Tin
sulfide using TA98, TA100, TA1535 and TA1537 strains of S. typhimurium
and WP2uvrA E. coli with and without metabolic activation was also
negative (Prochazkova, 2010). Tin disulfide and Tin sulfide showed a
comparable toxicological profile for this endpoint.
Aberration Test (in vitro):
key study for chromosome aberrations was done with a suspension of Tin
disulfide in cultured Chinese Hamster Ovary (CHO) cells, with and
without metabolic activation (S9 fraction) prepared from Aroclor 1254
induced rat liver (Indrani, 2012). In a preliminary toxicity test, Tin
disulfide showed evidence of significant growth inhibition at and above
229 µg/mL and 457 µg/mL during 3 hour exposure with and without S9,
respectively, whereas in the absence of S9 with 21-hour exposure, there
was evidence of significant reduction in the growth of CHO cells at and
above 229 µg/mL. Exposure of Tin disulfide did not cause any appreciable
change in the pH and osmolality of test solutions. In the definitive
chromosome aberration assay, CHO cells were exposed to the test item in
duplicate at concentrations of 23, 73 and 230 µg/mL (3 hours + S9 and 21
hours - S9) and at 30, 95 and 300 µg/mL (3 hours -S9). At the highest
concentration tested at 3 hours (230 and 300 µg/mL), the reduction in
the cell growth was 51% and 52% with and without S9, respectively,
whereas at 21 hours without S9 (230 µg/mL), the reduction in cell growth
was 53% when compared to the sterile water control. A total of 200
metaphases per dose level from duplicate cultures from the sterile water
control, each treatment group and the positive control were evaluate for
chromosome aberrations. There was no evidence of induction of chromosome
aberrations, including or excluding gaps, either in the presence or in
the absence of metabolic activation in any of these experiments. In each
of these experiments, under identical conditions, the respective
positive control substances produced a large and statistically
significant increase in aberrant metaphases. As a supporting study, the
clastogenicity potential of Tin sulfide was determined using In Vitro
Chromosome Aberration Test (Kovarik, 2010). The test was carried out in
human peripheral blood lymphocytes with and without metabolic activation
system in two separate assays. Tin sulfide did not induce an increase in
numerical and structural chromosome aberrations in cultured peripheral
blood lymphocytes. Further, an in vivo micronucleus test according to
OECD TG 474 was performed with Tin sulfide, also demonstrating absence
of micronuclei in the immature erythrocytes in the bone marrow
(Prochazkova, 2010). Tin disulfide and Tin sulfide showed a comparable
toxicological profile for this endpoint.
gene mutation Test (in vitro):
key gene mammalian mutation assay with Tin disulfide was conducted in
Chinese Hamster ovary (CHO) cells in the presence and absence of
metabolic activation system (S9 fraction) prepared from Aroclor 1254
induced rat liver (Bopanna, 2012). In a preliminary cytotoxicity test
Tin disulfide did not cause a significant cell growth inhibition as
evaluated by Relative Cloning efficiency (RCE) up to the highest tested
concentration of 1828.42 µg/mL (equivalent to 10 mM) with and without
S9. The test item formed precipitation of the test solution at and above
7 µg/mL but did not cause any appreciable change in the pH and
osmolality of the test solutions at the end of the 3-hour exposure to
treatment either in the presence or in the absence of metabolic
activation. In the initial gene mutation assay, CHO cells were exposed
at 58, 183, 578 and 1828 µg/mL for 3 hours with and without S9; in the
confirmatory gene mutation assay concentrations of 68, 203, 609 and 1828
µg/mL were applied for 3 hours with and without S9. There was no
evidence of induction of gene mutations in any of the test material
treated cultures either in the presence or absence of metabolic
activation. The results of the forward gene mutation assay at the hprtlocus
with Tin disulfide indicate that under the conditions of this study, the
test item was non-mutagenic when evaluated in the presence or absence of
Erythrocyte Micronucleus Test (in vivo):
potential of read-across substance Tin sulfide to cause cytogenetic
damage was assessed in a Mammalian Erythrocyte Micronucleus Test
according to OECD guideline 474.
No changes in health status and condition of the animals in any of the
groups were recorded during the acclimation and during the study. No
significant changes of mean body weight were observed in the animals
during the study. All the values of number of NPCE in all dose groups
were within the reference range for negative control group. No
statistically significant higher values of number of NPCE in any of the
dose groups (up to 11 of micronuclei) as compared to negative control
group (up to 13 of micronuclei) were noted. Statistically significant
differences were observed in the positive control group (NPCE – up to 38
of micronuclei) as compared to control group.
Read-across substance Tin sulfide does not induce damage to the
chromosomes or the mitotic apparatus of erythroblasts.
description of key information: Key
studies for bacterial and mammalian mutagenicity and chromosome
aberrations were performed for Tin disulfide, all demonstrating absence
of genotoxic potential. In addition, supporting studies for read-across
substance Tin sulfide also showed absence of mutagenicity and chromosome
aberration in a bacterial reverse mutation and in vitro chromosome
aberration and in vivo Micronucleus assay.
adverse effect observed (negative)
classification and labelling is needed for genotoxicity (bacterial and
mammalian mutations; chromosome aberrations) for Tin disulfide according
to EU labelling regulations Commission Directive 93/21/EEC and CLP
regulation (No. 1272/2008 of 16 December 2008).
Information on Registered Substances comes from registration dossiers which have been assigned a registration number. The assignment of a registration number does however not guarantee that the information in the dossier is correct or that the dossier is compliant with Regulation (EC) No 1907/2006 (the REACH Regulation). This information has not been reviewed or verified by the Agency or any other authority. The content is subject to change without prior notice.Reproduction or further distribution of this information may be subject to copyright protection. Use of the information without obtaining the permission from the owner(s) of the respective information might violate the rights of the owner.
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