Use of this information is subject to copyright laws and may require the permission of the owner of the information, as described in the ECHA Legal Notice.
EC number: 457-310-8 | CAS number: 127733-97-5 PLATINUM(2+), TETRAAMMINE-, (SP-4-1)-, DIACETATE (9CI)
Table 1: Comet results (% tail intensity) for kidney.
Table 2: Comet results (% tail intensity) for liver.
Table 3: Comet results (% tail intensity) for glandular stomach.
Table 4: Comet results (% tail intensity) for duodenum.
Table 5: Historical data Comet assay Negative control
LiverTail Intensity (%)
Males and Females
DuodenumTail Intensity (%)
StomachTail Intensity (%)
KidneyTail Intensity (%)
Lower control limit
(95% control limits)
Upper control limit
SD = Standard deviation
n = Number of observations
Kidney: Historical control data from experiments performed in Feb 2012 – July 2019
Liver, Stomach, Duodenum: Historical control data from experiments performed in Jan 2018 – July 2019
Table 6: Historical data Comet assay Positive control (200 mg/kg bw EMS orally dosed for two consecutive days)
The potential for tetraammineplatinum dichloride to cause DNA damage was evaluated in a study following OECD 489 and according to GLP. Male Wistar rats (5/group) were given gavage doses of 250, 500 or 1000 mg/kg bw/day of the test item on three consecutive days, or a vehicle control. The concurrent positive control group received two doses of EMS (200 mg/kg bw/day). Comet analyses were conducted on preparations of liver, glandular stomach, duodenum and kidney tissues.
There was no increase in % tail intensity in the liver, glandular stomach or duodenum, indicating that the test item is not genotoxic to these tissues.
There was a statistically significant and dose-related increase (p < 0.001) in DNA damage seen in the analysis of the kidney tissue. The tail intensity in animals dosed with 500 mg/kg bw/day was 14.56%, and in animals receiving 1000 mg/kg bw/day was 12.59%. However, these tail intensity values fell within the 95% confidence limits of the historical control data (upper limit 25.55%). As such, this finding was considered to be equivocal evidence of a genotoxic effect. No toxicity was observed in histopathological examination of the kidney tissues, indicating that this can be excluded as an indirect cause of the reported DNA damage.
The in vivo clastogenicity of tetraammineplatinum dichloride, as evaluated by its ability to induce micronuclei in polychromatic erythrocytes, was assessed in a study following OECD 474 and according to GLP. Male Wistar rats (5/group) were given gavage doses of 250, 500 or 1000 mg/kg bw/day of the test item on three consecutive days, or a vehicle control. The concurrent positive control group received a single dose of cyclophosphamide. Bone marrow was harvested from the femurs and assessed for micronuclei.
There was a slight but not statistically significant increase in micronucleated polychromatic erythrocytes in all treatment groups, but the incidences fell within the 95% limits of the historical control data. On that basis, tetraammineplatinum dichloride was concluded to be non-genotoxic under the conditions of this assay.
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.
Welcome to the ECHA website. This site is not fully supported in Internet Explorer 7 (and earlier versions). Please upgrade your Internet Explorer to a newer version.
Close Do not show this message again