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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Toxicological information


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Administrative data

Description of key information

No data is available on the carcinogenic potential of MeaTG by the oral and inhalation routes.

In a non-standard study by dermal route, sodium mercaptoacetate was administered to mice as 0, 1.0 and 2.0% solutions, until all animals died. Differences in the life span and the incidence of neoplasms between experimental and negative control mice were not statistically significant.

Key value for chemical safety assessment

Carcinogenicity: via oral route

Endpoint conclusion
Endpoint conclusion:
no study available

Carcinogenicity: via inhalation route

Endpoint conclusion
Endpoint conclusion:
no study available

Carcinogenicity: via dermal route

Link to relevant study records
carcinogenicity: dermal
Type of information:
read-across based on grouping of substances (category approach)
Adequacy of study:
key study
Justification for type of information:
The read-across is a category approach based on the hypothesis that compounds in this category are transformed to a common compound. This approach serves to use existing data on genotoxicity, repeated-dose toxicity, and reproductive toxicity endpoints for substances in this category.
There are no relevant variations in properties among source substances and the same potency is predicted for all target substances. This is Scenario 5 of the RAAF . Substances ATG, MEATG, KTG, CaTG, and NaTG are different inorganic salts of a common acid, thioglycolic acid (TGA; synonym: 2- mercaptoacetic acid). They dissociate rapidly in aqueous media, e.g., the test organism, to the common thioglycolate anion and to their different counter ions. The water solubility of all category members is high, except for CaTG which is only moderately soluble in water.
In the repeated-dose toxicity studies with NaTG, specific toxicity is exerted via the well-investigated inhibition of mitochondrial fatty acid beta-oxidation by the thioglycolate (2-mercaptoacetate) anion 2,3,4. Inhibition of beta-oxidation leads to increased triglycerides and decreased acetyl-CoA in liver, and subsequently reduced gluconeogenesis. The latter presents as hypoglycaemia in NaTGtreated rats, which is aggravated by fasting (Grosdidier, 2011; Report No. 37043 TSR). This mode of action (MoA) is thought to mediate the acute oral toxicity in fasted rats observed with all category members.
It can be predicted with high confidence that the target substances will display the same MoA and lead to the same effects seen with NaTG.
For more detailed information please refer to section 13.2.
Reason / purpose for cross-reference:
read-across: supporting information
Key result
Dose descriptor:
Effect level:
18 mg/kg bw/day
Based on:
test mat.
Remarks on result:
not determinable due to absence of adverse toxic effects
corrected for molecular weight differences
In analogy to NaTG, MeaTG is considered non-carcinogenic via the dermal route.
Endpoint conclusion
Endpoint conclusion:
no adverse effect observed
Dose descriptor:
18 mg/kg bw/day
Study duration:

Justification for classification or non-classification

According to the available carcinogenicity data, no classification is warranted for mercaptoacetic acid and its salts.

Additional information

No carcinogenicity data is available on mercaptoacetic acid and its salts by the inhalation or oral routes. The information on the carcinogenicity potential of mercaptoacetic acid and its salts is limited to a study in mice by chronic cutaneous application of sodium mercaptoacetate.

The carcinogenicity of sodium mercaptoacetate was evaluated using 94 Swiss female mice (7 weeks old) from the Eppley colony. 0.02 ml of a 1.0 and 2.0 % solutions of sodium mercaptoacetate in acetone (equivalent to dose levels of 6.6 and 13.3 mg/kg bw) were applied twice per week to the shaved skin (interscapular region) of each of the 49 or 45 mice, respectively. Ninety-three mice served as negative controls. Positive control groups, 40 mice, were treated with 7,12-dimethylbenz-[a]-anthracene. None of the experimental or control mice survived beyond week 120 of treatment. Infectious diseases, such as pneumonia and hepatitis, occurred in a small number of animals, resulting in an increased number of deaths. Large numbers of neoplasms were observed in treated and negative control mice: lymphomas, pulmonary adenomas, hepatic hemangiomas, ovarian neoplasms, and dermal fibromas. Epidermal neoplasms were not observed. Differences in the incidence of neoplasms between experimental and negative control mice were not statistically significant. No significant decrease in the life span of mice in experimental groups was observed. The authors concluded that sodium mercaptoacetate was not carcinogenic (Stenback et al., 1977).