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Reaction mass of Cobaltate(2-), [2-[[[4-hydroxy-3-[[2-oxo-1-[(phenylamino)carbonyl]propyl]azo]phenyl]sulfonyl]amino]benzoato(3-)][2-[[2-hydroxy-5-[(phenylamino)sulfonyl]phenyl]azo]-3-oxo-N-phenylbutanamidato(2-)]-, disodium and Cobaltate(3-), bis[2-[[[4-hydroxy-3-[[2-oxo-1-[(phenylamino)carbonyl]propyl]azo]phenyl]sulfonyl]amino]benzoato(3-)]-, trisodium and sodium bis[2-[[2-hydroxy-5-[(phenylamino)sulphonyl]phenyl]azo]-3-oxo-N-phenylbutyramidato(2-)]cobaltate(1-)
EC number: 947-257-3 | CAS number: -
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- Aquatic toxicity
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Endpoint summary
Administrative data
Key value for chemical safety assessment
Genetic toxicity in vitro
Description of key information
No mutagenicity was observed with test item in the tested bacteria strains, under the AMES test experimental conditions.
Link to relevant study records
- Endpoint:
- in vitro gene mutation study in bacteria
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Study period:
- From August the 09th to October the 02nd, 1980
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- guideline study with acceptable restrictions
- Principles of method if other than guideline:
- Ames test
- GLP compliance:
- no
- Type of assay:
- bacterial reverse mutation assay
- Species / strain / cell type:
- S. typhimurium, other: TA 100, TA 1535, TA 98, TA 1538 and TA 1537
- Details on mammalian cell type (if applicable):
- - Storage conditions: -70 °C, in liquid nitrogen.
- Culture: 4.5 ml bacterial culture and 0.5 ml dimethylsulfoxide. - Species / strain / cell type:
- E. coli WP2 uvr A
- Details on mammalian cell type (if applicable):
- - Storage conditions: -70 °C, in liquid nitrogen.
- Culture: 4.5 ml bacterial culture and 0.5 ml dimethylsulfoxide. - Metabolic activation:
- with and without
- Metabolic activation system:
- rat liver metabolizing system
- Test concentrations with justification for top dose:
- 5, 15.8, 50, 158, 500, 1580, 5000 and 15800 µg/plate
- Untreated negative controls:
- yes
- Positive controls:
- yes
- Positive control substance:
- 3-methylcholanthrene
- benzo(a)pyrene
- other: N'-nitro-N-nitrosoguanidine and benzo[a]pyrene 4-,5-oxide // 2-aminoanthracene
- Details on test system and experimental conditions:
- METHOD OF APPLICATION: in agar (plate incorporation)
TEST CONDITIONS
- Bacterial suspension: 0.1 ml/plate, about 1.7 x 10^9 colony forming units per ml.
- Test solution: 0.01 to 0.1 ml
- S-9 Mix, or a solution of 150 mM KCl buffered with 10 mM Na phosphate at pH 7.4: 0.5 ml/plate
- Top Agar (45 °C): 2.0 ml/plate
- Temperature: 37 °C
- Time: 46 - 55 hours for TA 98 and WPr uvrA; 62 - 68 hours for all other strains.
- Other: in experiments in which epoxide hydratase was inhibited 0.3 µl 1,1,-trichloropropene 2,3-oxide in 10 µl DMSO. Respective plates without epoxide hydratase inhibition only received 10 µl DMSO.
REPLICATES: 2 replicates per dose per strain
PREPARATION OF TEST SOLUTION
- Solvent: H2O, positive controls in dimethylsulfoxide p.a.
- Amount per plate: 100 µl H2O, 10 to 30 µl dimethylsulfoxide, resp.
- Method for suspension of refractory substance: ultrasonication.
- Time of preparation: the day of the expertment.
SOFT AGAR
- Amount per plate: 2 ml
- Temperature: 45 °C
- Composition: 0.55 % Agar, 0.55 % NaCI, 25 mM Na phosphate ph 7.4, 50 µM histidine, 50 µM biotin and 50 µM tryptophan.
TOXICITY TEST
To estimate toxicity, his+ bacteria, about 600 colony forming units, were added as an internal standard to otherwise normal mutagenicity plates. The his+ bacteria used were spontaneous revertants from TA 1537. They were added to plates together with a strain which gives low numbers of revertant colonies (TA 1537). The difference in the number of colonies on plates with and without added his+ bacteria, in the presence of test compound, is compared to the value obtained with solvent controls. The ratio of these two values gives the relative survival rate. In tests where generation ard selection of mutants are not separated, as in the standard Ames test, relative survival rates cannot be used for correcting the number of revertant colonies for toxic effects. However, since toxicity reduces the sensitivity of the test, a measure for toxicity is required for validation of mutagenicity data.
The relative survival rate is more objective and far more sensitive criterion than mere observation of the his- background lawn.
RAT LIVER METABOLIZING SYSTEM
For all experiments fresh tissue preparations from animals sacrificed on the day of the experiment were used.
Male rats (8-13 weeks old, ca 200-300 g), Sprague Dawley, were used. Aroclor 1254 was administrated intraperitoeally. Sunflower oil was used as solvent (4 vol per 1 vol Aroclor 12541). 500 mg Aroclor 1254 per kg body weight was administrated by a sigle application, 6 days before sacrifice.
Composition of S9 mix: S9 0.33 ml, MgCl2 8 µmol, KCl 33 µmol, glucose-6-phosphate 5 µmol, NADP+ 4 µmol, Na-phosphate 50 µmol; pH 7.4 - 7.5. - Species / strain:
- S. typhimurium, other: TA 100, TA 1535, TA 98, TA 1538 and TA 1537
- Metabolic activation:
- with and without
- Genotoxicity:
- negative
- Cytotoxicity / choice of top concentrations:
- cytotoxicity
- Untreated negative controls validity:
- valid
- Positive controls validity:
- valid
- Additional information on results:
- No mutagenicity was observed with test item under any experimental condition. Because in the first experiment for direct mutagenicity the number of revertant colonies from TA 98 was slightly (less than two-fold) increased on some plates with test item, this part of the experiment was repeated with a larger number of parallel plates. The negative result of the repeated experiment strongly supported the interpretation that the marginal effect of the first experiment was simply due to dispersion rather than to a real effect. Mutagenicity effects were also not observed when the epoxide hydratase inhibitor and glutathione depletory 1,1,1-trichloropropene 2,3-oxide was added to the S-9 Mix in order to increase the sensitivity of the test towards compounds which are activated to mutagenic epoxides (this experiment was performed with TA 98).
CITOTOXICITY
For determination of toxicity his+ mutants were added to some plates in order to estimate the survival of mutants. In the absence of S-9 Mix the compound started to be noticeably toxic at 500 µg. At this and at the next higher dose (1580 µg) sufficient bacteria survived that there is a good chance that relatively stable mutagens still may be detected. In the presence of S-9 Mix, toxicity was much lower. Only at 15800 µg a substantial decrease in survival occurred. All in all, toxicity and solubility of compound are such that it can be tested for mutagenicity with a good sensitivity.
CONTROLS
In the study, N-methyl-N'-nitro-N-nitrosoguanidine and benzo(a)pyrere 4,5-oxide showed potent mutagenic effects in the absence of S9 Mix. With TA 100 and TA 1537, strains in which the mutagenicity of these compounds is seen well, tests were also performed in the presence of S-9 Mix.
S-9 Mix completely prevented the mutagenic effects indicating the functioning of drug-metabolizing enzymes which play an inactivating role with the compounds urder investigation (but may activate other compounds). Metabolic activity of S-9 Mix is furthermore shown by the strong mutagenic effects of the activation-requiring mutagens in the presence of S-9 Mix, whereas these compounds were inactive or at most marginally active in the direct test (the direct tests were only performed with the most sensitive strains TA 98 and TA 100). Benzo(a)pyrene is activated well by liver preparations from 3-methylcholanthrene-treated rats, but only poorly by preparations from phenobarbital-treated animals. The reverse is true for 3-methylcholanthrene.
Aroclor 1254 induces monooxygenases which are induced by phenobarbital as well as those which are induced by 3-methylcholanthrene. Both benzo(a)pyrene and 3-methylcholanthrene were activated in the experiments. This indicates that both metabolizing systems were functioning. Also 2-aminoanthracene, which requires N-oxidation for activation, was strongly mutagenic. This compound is mutagenic in all strains employed. For simplicity the study director used the same dose with all strains, although the maximal effects occur at different doses due to differences in permeability and toxicity among the strains. Maximal effects with TA 1538 would be seen at lower doses, with WP2 uvrA at higher doses than those used.
Inhibition of epoxide hydratase by 1,1,1-trichloropropene oxide was controlled by studying its effect on the mutagenicity of benzo(a)pyrene. 1,1,1-trichloropropene oxide increased the mutagenicity of benzo(a)pyrene several fold. - Conclusions:
- No mutagenicity was observed with test item under any experimental condition.
- Executive summary:
The test item was tested for mutagenicity with Salmonella typhimurium TA 1535, TA 100, TA 1537, TA 1538 and TA 98 and with Escherichia coli WP2 uvrA, both directly and in the presence of a mammalian metabolizing system. Eight different concentrations from 5 to 15800 µg per plate were used. The compound was dissolved in H2O at 70 °C. When the solution was added to the plate, part of the test compound precipitated at the two highest doses. Some precipitate was still present at the end of the experiment.
For determination of toxicity his+ mutants were added to some plates in order to estimate the survival of mutants. In the absence of S-9 Mix the compound started to be noticeably toxic at 500 µg. At this and at the next higher dose (1580 µg) sufficient bacteria survived that there is a good chance that relatively stable mutagens still may be detected. In the presence of S-9 Mix, toxicity was much lower. Only at 15800 µg a substantial decrease in survival occurred. All in all, toxicity and solubility of compound are such that it can be tested for mutagenicity with a good sensitivity.
No mutagenicity was observed with test item under any experimental condition. Because in the first experiment for direct mutagenicity the number of revertant colonies from TA 98 was slightly (less than two-fold) increased on some plates with test item, this part of the experiment was repeated with a larger number of parallel plates. The negative result of the repeated experiment strongly supported the interpretation that the marginal effect of the first experiment was simply due to dispersion rather than to a real effect. Mutagenicity effects were also not observed when the epoxide hydratase inhibitor and glutathione depletory 1,1,1-trichloropropene 2,3-oxide was added to the S-9 Mix in order to increase the sensitivity of the test towards compounds which are activated to mutagenic epoxides (this experiment was performed with TA 98).
The positive controls confirmed the suitability of the system.
Conclusion
No mutagenicity was observed with test item under any experimental condition.
Reference
AMES test with S-9 mix
Dose µg/plate | Solvent | Relative Survival Rate | TA 100 | TA 1535 | WP2 uvrA | TA 98 | TA 98 TCPO | TA 1538 | TA 1537 | |||||||
0 | 100 µl H2O | 1.0 | 137 | 125 | 15 | 14 | 39 | 41 | 30 | 22 | 37 | 31 | 21 | 34 | 21 | 19 |
0 | 100 µl | 1.0 | 145 | 141 | 7 | 9 | 37 | 48 | 24 | 33 | 25 | 30 | 27 | 30 | 24 | 23 |
5 | 0.9 | 115 | 140 | 10 | 18 | 19 | 19 | 19 | 18 | 27 | 24 | 37 | 22 | 28 | 24 | |
Test item 15.8 | 100µl H2O | 1.0 | 141 | 109 | 12 | 10 | 30 | 23 | 29 | 28 | 37 | 33 | 26 | 30 | 19 | 16 |
Test item 50 | 100 µl | 1.0 | 144 | 128 | 12 | 19 | 33 | 32 | 24 | 21 | 34 | 40 | 26 | 27 | 19 | 25 |
Test item 158 | 100 µl | 1.0 | 152 | 154 | 14 | 17 | 50 | 44 | 21 | 30 | 45 | 41 | 33 | 23 | 29 | 30 |
Test item 500 | 100 µl | 1.0 | 104 | 117 | 6 | 15 | 40 | 51 | 30 | 20 | 23 | 23 | 26 | 22 | 34 | 23 |
Test item 1580 | 100 µl | 1.0 | 102 | 124 | 12 | 7 | 61 | 35 | 27 | 20 | 21 | 7 | 14 | 14 | 18 | 18 |
Test item 5000 ** | 100 µl * | 0.8 | 100 | 99 | 9 | 10 | 46 | 48 | 7 | 7 | 2 | 6 | 9 | 6 | 13 | 13 |
Test item 15800 ** | 100 µl * | 0.03 | 24 | 14 | 4 | 0 | 58 | 32 | 0 | 0 | 0 | 0 | 0 | 0 | 4 | 1 |
Benzo(a)pyrene 10 | 10 µl DMSO | 0.7 | 1050 | 1140 | 21 | 27 | 78 | 74 | 574 | 601 | 950 | 970 | 270 | 266 | 166 | 144 |
Benzo(a)pyrene 50 | 10 µl | 1.0 | 376 | 391 | 13 | 15 | 42 | 42 | 63 | 72 | 427 | 453 | 50 | 33 | 79 | 77 |
2-Aminoanthracene 10 | 10 µl | 0.6 | 4500 | 4400 | 242 | 236 | 149 | 143 | 4050 | 5100 | 3600 | 3700 | 1136 t | 716 t | 182 | 199 |
3-methylcholanthrene 90 | 30 µl | 0.9 | 3800 | 3700 | 10 | 5 | 49 | 51 | 1090 | 1310 | 1160 | 1680 | 255 | 293 | 91 | 109 |
Benzo(a)pyrene 4,5-oxide | 10 µl | 1.0 | 143 | 139 | 25 | 18 | ||||||||||
N-methyl-N'-nitro-N-nitrosogunidine | 10 µl | 1.2 | 152 | 154 | 27 | 19 |
t: 2-Aminoanthracene showed stronger toxicity with TA 1538 than with all other strains and noticeably reduced at the his- background law in this strain
**macroscopically visible precipitate of test compound on the plate.
* The conpound was dissolved in H2O at 70 °C before being added to the plate.
AMES test withou S-9 mix
Dose µg/plate | Solvent | Relative Survival Rate | TA 100 | TA 1535 | WP2 uvrA | TA 98 exp.1 | TA 98 exp.2 | TA 1538 | TA 1537 | ||||||||
0 | 100µl H2O | 1.0 | 90 | 89 | 14 | 12 | 50 | 49 | 26 | 27 | 32 | 32 | 32 | 13 | 16 | 9 | 8 |
0 | 100 µl | 1.0 | 96 | 108 | 16 | 14 | 49 | 48 | 25 | 18 | 32 | 27 | 26 | 14 | 15 | 12 | 14 |
5 | 0.9 | 72 | 81 | 16 | 18 | 32 | 73 | 28 | 38 | 33 | 27 | 30 | 21 | 19 | 11 | -* | |
Test item 15.8 | 100µl H2O | 1.0 | 103 | 90 | 16 | 18 | 45 | 53 | 31 | 44 | 37 | 27 | 38 | 20 | 24 | 8 | 12 |
Test item 50 | 100 µl | 0.8 | 88 | 106 | 13 | 17 | 39 | 49 | 41 | 48 | 39 | 29 | 28 | 24 | 18 | 8 | 10 |
Test item 158 | 100 µl | 0.8 | 92 | 89 | 13 | 21 | 39 | 37 | 19 | 27 | 24 | 28 | 35 | 8 | 14 | 5 | 14 |
Test item 500 | 100 µl | 0.5 | 43 | 49 | 8 | 13 | 43 | 40 | 25 | 22 | 24 | 20 | 29 | 3 | 7 | 4 | 4 |
Test item 1580 | 100 µl | 0.2 | 24 | 29 | 9 | 7 | 50 | 39 | 9 | 16 | 8 | 10 | 11 | 0 | 3 | 0 | 0 |
Test item 5000 ** | 100 µl * | 0.0 | 0 | 0 | 3 | 1 | 41 | 54 | 0 | 0 | 0 | 0 | 0 | 0 | |||
Test item 15800 ** | 100 µl * | 0.0 | 0 | 0 | 0 | 0 | 47 | 56 | 0 | 0 | 0 | 0 | 0 | 0 | |||
Benzo(a)pyrene 10 | 10 µl DMSO | 1.1 | 76 | 105 | 35 | 26 | |||||||||||
Benzo(a)pyrene 50 | 10 µl | 1.0 | 88 | 82 | 22 | 25 | |||||||||||
2-Aminoanthracene 10 | 10 µl | 1.1 | 116 | 123 | 41 | 56 | |||||||||||
3-methylcholanthrene 90 | 30 µl | 1.0 | 164 | 161 | 80 | 65 | |||||||||||
Benzo(a)pyrene 4,5-oxide | 10 µl | 1.0 | 2200 | 2250 | 21 | 19 | 63 | 65 | 4000 | 3900 | 1520 | 1610 | 1680 | 693 | 720 | 539 | 532 |
N-methyl-N'-nitro-N-nitrosogunidine | 10 µl | 0.7 | 19000 | 13000 | 36000 | 33000 | 418 | 433 | 101 | 95 | 60 | 63 | 58 | 16 | 16 | 129 | 62 |
-*: plate contaminated; not tested
**macroscopically visible precipitate of test compound on the plate.
* The conpound was dissolved in H2O at 70 °C before being added to the plate.
Endpoint conclusion
- Endpoint conclusion:
- no adverse effect observed (negative)
Additional information
IN VITRO GENE MUTATION TEST IN BACTERIA
The test item was tested for mutagenicity with Salmonella typhimurium TA 1535, TA 100, TA 1537, TA 1538 and TA 98 and with Escherichia coli WP2 uvrA, both directly and in the presence of a mammalian metabolizing system. Eight different concentrations from 5 to 15800 µg per plate were used. The compound was dissolved in H2O at 70 °C. When the solution was added to the plate, part of the test compound precipitated at the two highest doses. Some precipitate was still present at the end of the experiment.
For determination of toxicity his+ mutants were added to some plates in order to estimate the survival of mutants. In the absence of S-9 Mix the compound started to be noticeably toxic at 500 µg. At this and at the next higher dose (1580 µg) sufficient bacteria survived that there is a good chance that relatively stable mutagens still may be detected. In the presence of S-9 Mix, toxicity was much lower. Only at 15800 µg a substantial decrease in survival occurred. All in all, toxicity and solubility of compound are such that it can be tested for mutagenicity with a good sensitivity.
No mutagenicity was observed with test item under any experimental condition. Because in the first experiment for direct mutagenicity the number of revertant colonies from TA 98 was slightly (less than two-fold) increased on some plates with test item, this part of the experiment was repeated with a larger number of parallel plates. The negative result of the repeated experiment strongly supported the interpretation that the marginal effect of the first experiment was simply due to dispersion rather than to a real effect. Mutagenicity effects were also not observed when the epoxide hydratase inhibitor and glutathione depletory 1,1,1-trichloropropene 2,3-oxide was added to the S-9 Mix in order to increase the sensitivity of the test towards compounds which are activated to mutagenic epoxides (this experiment was performed with TA 98).
The positive controls confirmed the suitability of the system.
Since the Acid Yellow 235 lot tested in the key study was characterized by an appreciable non-hazardous impurity content, the available data on structural analogous Similar Substance 01 has been taken into account, in order to confirm the study outcomes. The read across approach can be considered as reliable and adequate for the purpose; details and explanations are detailed in the report attached to the IUCLID section 13.2.
The study was performed to investigate the potential of Similar Substance 01 to induce gene mutations according to the plate incorporation test and the pre-incubation test using the Salmonella typhimurium strains TA 1535, TA 1537, TA 98, and TA 100. The assay was performed in two independent experiments, both with and without liver microsomal activation, at the following concentrations: 33.3; 100.0; 333.3; 1000.0; 2500.0; and 5000.0 µg/plate.
Slight toxic effects, evident as a reduction in the number of revertants, occurred in strains TA 1535 and TA 1537 without metabolic activation (S9 mix) in the first experiment.
The plates incubated with the test article showed normal background growth up to 5000.0 µg/plate with and without S9 mix in all strains used.
No relevant increases in revertant colony numbers of any of the four tester strains were observed following treatment with test item at any dose level, either in the presence or absence of metabolic activation (S9 mix). There was also no tendency of higher mutation rates with increasing concentrations in the range below the generally acknowledged border of biological relevance.
Appropriate reference mutagens were used as positive controls and showed a distinct increase of induced revertant colonies.
It was concluded that during the described mutagenicity test and under the experimental conditions reported, the test article did not induce gene mutations by base pair changes or frameshifts in the genome of the strains used.
Justification for classification or non-classification
According to the CLP Regulation (EC) No 1272/2008, for the purpose of the classification for germ cell mutagenicity, substances are allocated in one of two categories in consideration of the fact that they are:
- substances known to induce heritable mutations or to be regarded as if they induce heritable mutations in the germ cells of humans or substances known to induce heritable mutations in the germ cells of humans or
- substances which cause concern for humans owing to the possibility that they may induce heritable mutations in the germ cells of humans.
The available information suggest that test substance did not show any reasons of concern from the genotoxicity point of view.
In conclusion, the substance does not meet the criteria to be classified for genetic toxicity according to the CLP Regulation (EC) No 1272/2008.
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