N-(1-oxotetradecyl)sarcosine

Endpoint summary

Key value for chemical safety assessment

Genetic toxicity in vitro

Description of key information

Bacterial Mutagenicity (key, OECD 471), Ames: negative with and without metabolic activation

Mammalian Cytogenicity (WoE, OECD 473), Chromosome Aberration: negative with and without metabolic activation

RA from source substances N-methyl-N-[C18-(unsaturated)alkanoyl]glycine (EC 701-177-3), Sodium N-lauroylsarcosinate (CAS 137-16-6) and Sodium N-methyl-N-(1-oxotetradecyl)aminoacetate (CAS 30364-51-3)

Mammalian Mutagenicity (WoE, OECD 476): negative with and without metabolic activation

RA from source substances N-methyl-N-[C18-(unsaturated)alkanoyl]glycine (EC 701-177-3), Sodium N-lauroylsarcosinate (CAS 137-16-6) and Sodium N-methyl-N-(1-oxotetradecyl)aminoacetate (CAS 30364-51-3)

Link to relevant study records

Reference

Reference 1

Endpoint:

in vitro cytogenicity / chromosome aberration study in mammalian cells

Type of information:

read-across from supporting substance (structural analogue or surrogate)

Remarks:

Summary of available data used for the endpoint assessment of the target substance

Adequacy of study:

weight of evidence

Justification for type of information:

Please refer to analogue justification report provided in IUCLID section 13

Reason / purpose for cross-reference:

read-across source

Reason / purpose for cross-reference:

read-across source

Reason / purpose for cross-reference:

read-across source

Key result

Species / strain:

lymphocytes: in whole blood treated with heparin

Metabolic activation:

with and without

Genotoxicity:

negative

Cytotoxicity / choice of top concentrations:

cytotoxicity

Remarks:

from 30 µg/mL without and from 40 µg/mL with metabolic activation

Vehicle controls validity:

valid

Untreated negative controls validity:

not applicable

Positive controls validity:

valid

Remarks on result:

other: Source: EC 701-177-3, LAUS, 2010

Additional studies taken into account in the Weight-of-Evidence approach:

CAS 137-16-6, Harlan, 2010a: not clastogenic (lymphocytes)

CAS 30364-51-3, Harlan, 2013a: not clastogenic (lymphocytes)

Conclusions:

Interpretation of results: negative

Reference 2

Endpoint:

in vitro gene mutation study in mammalian cells

Type of information:

read-across from supporting substance (structural analogue or surrogate)

Remarks:

Summary of available data used for the endpoint assessment of the target substance

Adequacy of study:

weight of evidence

Justification for type of information:

Please refer to analogue justification report provided in IUCLID section 13

Reason / purpose for cross-reference:

read-across source

Reason / purpose for cross-reference:

read-across source

Reason / purpose for cross-reference:

read-across source

Key result

Species / strain:

Chinese hamster lung fibroblasts (V79)

Metabolic activation:

with and without

Genotoxicity:

negative

Cytotoxicity / choice of top concentrations:

cytotoxicity

Remarks:

at ≥4 µg/mL (experiment I, -S9), ≥ 48 µg/mL (experiment I,+ S9); 96 µg/mL (experiment II, -S9, 24 h), 56 µg/mL (experiment II, +S9, 4 h)

Vehicle controls validity:

valid

Untreated negative controls validity:

not applicable

Positive controls validity:

valid

Remarks on result:

other: Source: EC 701-177-3, Harlan, 2010b

Additional studies taken into account in the Weight-of-Evidence approach:

CAS 137-16-6, Harlan, 2010c: negative (mouse lymphoma L5178Y)

CAS 30364-51-3, Harlan, 2013b: negative (mouse lymphoma L5178Y TK +/- cells)

Conclusions:

Interpretation of results: negative

Reference 3

Endpoint:

in vitro gene mutation study in bacteria

Type of information:

experimental study

Adequacy of study:

key study

Study period:

03 Oct 2012 - 30 Nov 2012

Reliability:

1 (reliable without restriction)

Rationale for reliability incl. deficiencies:

guideline study

Qualifier:

according to guideline

Guideline:

OECD Guideline 471 (Bacterial Reverse Mutation Assay)

Version / remarks:

(adopted 21 July 1997)

Deviations:

no

Qualifier:

according to guideline

Guideline:

EU Method B.13/14 (Mutagenicity - Reverse Mutation Test Using Bacteria)

Version / remarks:

(adopted 30 May 2008)

Deviations:

no

GLP compliance:

yes (incl. QA statement)

Remarks:

The Department of Health of the Government of the United Kingdom

Type of assay:

bacterial reverse mutation assay

Target gene:

his operon (S. typhimurium strains)
trp operon (E. coli)

Species / strain / cell type:

other: TA 1535, TA 1537, TA98, and TA100

Species / strain / cell type:

E. coli WP2 uvr A

Metabolic activation:

with and without

Metabolic activation system:

cofactor supplemented post-mitochondrial fraction (S9 mix), prepared from the livers of rats treated with Phenobarbitone/beta-Naphthoflavone

Test concentrations with justification for top dose:

- Preliminary Toxicity Test:
TA100 or WP2uvrA: 0.15, 0.5, 1.5, 5, 15, 50, 150, 500, 1500 and 5000 μg/plate
- Mutation Test - Experiment 1
All Salmonella strains (with and without S9-mix): 5, 15, 50, 150, 500, 1500 and 5000 μg/plate
WP2uvrA (with and without S9-mix): 50, 150, 500, 1500 and 5000 μg/plate
- Mutation Test - Experiment 2
All Salmonella strains (with and without S9-mix): 1.5, 5, 15, 50, 150 and 500 μg/plate
WP2uvrA (with and without S9-mix): 15, 50, 150, 500, 1500 and 5000 μg/plate

Vehicle / solvent:

- Vehicle used: DMSO
- Justification for choice of vehicle: based on solubility checks performed in-house (The test item was insoluble in sterile distilled water and acetonitrile at 50 mg/mL, acetone at 100 mg/mL and THF at 200 mg/mL but was noted to be soluble in DMSO and dimethyl formamide at 50 mg/mL)

Untreated negative controls:

no

Negative solvent / vehicle controls:

yes

True negative controls:

no

Positive controls:

yes

Positive control substance:

4-nitroquinoline-N-oxide

9-aminoacridine

N-ethyl-N-nitro-N-nitrosoguanidine

Remarks:

- S9: N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG): 2 μg/plate (WP2uvrA), 3 μg/plate (TA100), 5 μg/plate (TA1535); 9-Aminoacridine (9AA): 80 μg/plate (TA1535), 4-Nitroquinoline-1-oxide (4NQO): 0.2 μg/plate (TA98)

Untreated negative controls:

no

Negative solvent / vehicle controls:

yes

True negative controls:

no

Positive controls:

yes

Positive control substance:

benzo(a)pyrene

other: 2-Aminoanthracene

Remarks:

+ S9: 2-Aminoanthracene (2AA): 1 μg/plate (TA100), 2 μg/plate (TA1535 and TA1537), 10 μg/plate (WP2uvrA); Benzo(a)pyrene (BP): 5 μg/plate (TA98)

Details on test system and experimental conditions:

METHOD OF APPLICATION: plate incorporation (Experiment 1) and pre-incubation (Experiment 2)

DURATION
- Preincubation period: 20 min
- Exposure duration: 48 h

NUMBER OF REPLICATIONS: triplicates each in two independent experiments

DETERMINATION OF CYTOTOXICITY
- Method: reduction in the number of revertant colonies, a clearing or diminution of the background lawn (Preliminary Toxicity Test)

Evaluation criteria:

There are several criteria for determining a positive result. Any, one, or all of the following can be used to determine the overall result of the study:
1. A dose-related increase in mutant frequency over the dose range tested (De Serres and Shelby (1979)).
2. A reproducible increase at one or more concentrations.
3. Biological relevance against in-house historical control ranges.
4. Statistical analysis of data as determined by UKEMS (Mahon et al (1989)).
5. Fold increase greater than two times the concurrent solvent control for any tester strain (especially if accompanied by an out-of-historical range response).
A test item will be considered non-mutagenic (negative) in the test system if the above criteria are not met.
Although most experiments will give clear positive or negative results, in some instances the data generated will prohibit making a definite judgement about test item activity. Results of this type will be reported as equivocal.

Species / strain:

S. typhimurium, other: TA 1535, TA 1537, TA 98 and TA 100

Metabolic activation:

with and without

Genotoxicity:

negative

Cytotoxicity / choice of top concentrations:

cytotoxicity

Remarks:

Preliminary Toxicity Test: TA100 at 500 μg/plate and above (+ and - S9); plate incorporation Experiment: all strains at 500 μg/plate and above (+S9) and 1500 µg/plate (- S9); pre-incubation Experiment: all strains at 150 μg/plate and above (+ and - S9)

Vehicle controls validity:

valid

Untreated negative controls validity:

not examined

Positive controls validity:

valid

Species / strain:

E. coli WP2 uvr A

Metabolic activation:

with and without

Genotoxicity:

negative

Cytotoxicity / choice of top concentrations:

cytotoxicity

Remarks:

pre-incubation Experiment: at 5000 μg/plate (+ and - S9)

Vehicle controls validity:

valid

Untreated negative controls validity:

not examined

Positive controls validity:

valid

Additional information on results:

TEST-SPECIFIC CONFOUNDING FACTORS
- Precipitation: none
- Other confounding effects: none reported

RANGE-FINDING/SCREENING STUDIES: Range finding test: in order to select the appropriate dose levels for use in the main test, a preliminary test was carried out to determine the toxicity of the test substance. Ten concentrations of the test item formulation (0.15, 0.5, 1.5, 5, 15, 50, 150, 500, 1500 and 5000 µg/plate) and vehicle control (DMSO) were tested.
The test item was toxic to TA 100 from 500 µg/plate and non-toxic to WP2 uvrA.


COMPARISON WITH HISTORICAL CONTROL DATA: The results of the vehicle and positive controls (+ and - S9) are within the historical control data of the last two years.

Table 1 Test Results: Experiment 1 (plate incorporation) – Without Metabolic Activation

Test group		Number of revertants (mean) ± SD
		Base-pair substitution strains			Frameshift strains
		TA100	TA1535	WP2uvrA	TA98	TA1537
Solvent control		108±14.2	22±2.6	21±4.4	25±9.3	11±1.5
Test item	5 µg/plate	107±22.77	20±4.2	N/T	27±10.1	11±0.0
	15 µg/plate	108±26.0	17±4.0	N/T	19±5.6	9±0.6
	50 µg/plate	109±11.3	19±0.6	23±3.5	25±0.0	10±1.2
	150 µg/plate	92±26.8	17±1.5	20±4.5	15±5.2	10±1.2
	500 µg/plate	115±14.3(S)	11±3.2 (S)	16±4.0	13±3.2 (S)	2±1.2 (V)
	1500 µg/plate	0±0 (V)	0±0(V)	16±3.0	0±0 (V)	0±0(V)
	5000 µg/plate	0±0 (V)	0±0(V)	16±0.6	0±0 (T)	0±0(T)
Positive controls S9 mix (-)	Name Dose Level No. of Revertants	ENNG	ENNG	ENNG	ENNG	ENNG
		3 µg	5 µg	2 µg	0.2 µg	80 µg
		622±19.4	2560±480.1	795±36.1	174±66.4	655±91.3

Table 2 Test Results: Experiment 1 (plate incorporation) – With Metabolic Activation

Test group		Number of revertants (mean) ± SD
		Base-pair substitution strains			Frameshift strains
		TA100	TA1535	WP2uvrA	TA98	TA1537
Solvent control		118±10.1	15±3.5	25±6.0	25±4.4	11±1.5
Test item	5 µg/plate	92±6.8	14±1.2	N/T	24±7.0	10±1.7
	15 µg/plate	96±9.5	12±4.2	N/T	24±6.9	10±2.1
	50 µg/plate	93±15.3	16±1.0	24±8.5	20±4.0	11±3.2
	150 µg/plate	104±9.6	11±2.9	20±6.4	23±9.0	10±2.9
	500 µg/plate	64±20.0	11±0.6	24±2.3	17±5.3	6±1.2
	1500 µg/plate	0±0 (V)	0±0 (V)	26±6.2	3±1.5 (S)	0±0 (V)
	5000 µg/plate	0±0(V)	0±0 (T)	16±2.3	0±0 (V)	0±0 (V)
Positive controls S9 mix (+)	Name Dose Level No. of Revertants	2AA	2AA	2AA	BP	2AA
		1 µg	2 µg	10 µg	5 µg	2 µg
		675±24.4	171±6.1	195±17.9	142±17.2	452±111.9

Table 3 Test Results: Experiment 2 (pre-incubation) – Without Metabolic Activation

Test group		Number of revertants (mean) ± SD
		Base-pair substitution strains			Frameshift strains
		TA100	TA1535	WP2uvrA	TA98	TA1537
Solvent control		109±12.1	21±1.5	20±1.5	19±1.5	10±1.5
Test item	1.5 µg/plate	147±51.9	16±1.5	N/T	13±0.6	11±1.2
	5 µg/plate	118±5.1	19±1.7	N/T	17±2.3	11±2.0
	15 µg/plate	171±90.1	20±1.2	20±1.0	19±0.6	10±3.8
	50 µg/plate	92±3.5	19±0.6	15±0.6	14±1.2	10±2.3
	150 µg/plate	58±17.5 (S)	9±2.5 (S)	19±2.6	12±3.1 (S)	7±2.0 (S)
	500 µg/plate	0±0 (V)	0±0 (T)	15±5.1	0±0 (T)	0±0 (T)
	1500 µg/plate	0±0 (T)	0±0 (T)	13±4.2	0±0 (T)	0±0 (T)
	5000 µg/plate	N/T	N/T	12±0.6 (S)	N/T	N/T
Positive controls S9 mix (-)	Name Dose Level No. of Revertants	ENNG	ENNG	ENNG	4NQO	9AA
		3 µg	5 µg	2 µg	0.2 µg	80 µg
		571±60.7	843±81.6	159±17.3	335±154.8	622±53.3

Table 4 Test Results: Experiment 2 (pre-incubation) – With Metabolic Activation

Test group		Number of revertants (mean) ± SD
		Base-pair substitution strains			Frameshift strains
		TA100	TA1535	WP2uvrA	TA98	TA1537
Solvent control		108±7.2	16±2.5	18±1.5	28±3.5	11±1.5
Test item	1.5 µg/plate	115±2.9	15±0.6	N/T	26±2.5	9±4.0
	5 µg/plate	98±19.3	15±4.2	N/T	31±3.2	9±2.0
	15 µg/plate	106±10.1	12±1.5	20±2.0	26±4.6	12±1.2
	50 µg/plate	106±6.1	16±3.8	15±0.6	24±5.7	10±1.0
	150 µg/plate	81±3.1	15±1.2 (S)	17±1.2	13±1.2	2±1.0 (S)
	500 µg/plate	0±0 (V)	0±0 (V)	19±2.3	0±0 (V)	0±0 (V)
	1500 µg/plate	0±0 (T)	0±0 (T)	20±4.2	0±0 (V)	0±0 (T)
	5000 µg/plate	N/T	N/T	13±3.5 (S)	N/T	N/T
Positive controls S9 mix (+)	Name Dose Level No. of Revertants	2 AA	2 AA	2 AA	BP	2 AA
		1 µg	2 µg	10 µg	5 µg	2 µ
		1015±60.7	474±199.8	171±7.4	276±23.5	132±19.5

N/T Not tested at this dose level

(S) = Sparse bacterial background lawn

(V) = Very weak bacterial background lawn

(T) = Toxic, no bacterial background lawn

solvent control:DMSO

positive controls (- S9):

-N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG): 2 μg/plate (WP2uvrA), 3 μg/plate (TA100), 5 μg/plate (TA1537)

 

Conclusions:

Interpretation of results: negative

Endpoint conclusion

Endpoint conclusion:

no adverse effect observed (negative)

Genetic toxicity in vivo

Endpoint conclusion

Endpoint conclusion:

no study available

Additional information

Only data on gene mutation in bacteria are available for N-(1-oxotetradecyl)sarcosine (CAS 52558-73-3). Therefore, a Weight-of-Evidence approach referring to the analogue substances N-methyl-N-[C18-(unsaturated)alkanoyl]glycine (EC 701-177-3), Sodium N-lauroylsarcosinate (CAS 137-16-6) and Sodium N-methyl-N-(1-oxotetradecyl)aminoacetate (CAS 30364-51-3) was applied to derive information on the ability of the registered substance to induce chromosome aberrations and gene mutation in mammalian cells.

Genetic toxicity (mutagenicity) in bacteria in vitro

A bacterial gene mutation assay (Ames test) was performed with N-(1-oxotetradecyl)sarcosine (CAS 52558-73-3) according to OECD TG 471 and under GLP conditions (Harlan, 2013a). The strains S. typhimurium TA 1535, TA 1537, TA 98 and TA 100 and E. coli WP2 uvr A were tested according to the plate incorporation and pre-incubation procedures in the absence and presence of a metabolic activation system (Phenobarbitone/beta-Naphthoflavone-induced rat liver S9-mix). The study was conducted in 3 repetitions in two independent experiments at concentrations from 5 to 5000 µg/plate (vehicle: DMSO). Adequate solvent and positive controls were included in the experiment. No increase in the number of revertant colonies was noted in any of the bacterial strains, with and without metabolic activation system. Cytotoxicity was observed at 500 µg/plate and higher concentrations (S. typhimurium strains) and in the highest dose tested (E. coli strain) with and without metabolic activation. The included solvent and positive controls showed the expected results, thus demonstrating the validity of the test and the activity of the metabolising system. Under the conditions of the study, the test substance did not induce mutations in the bacterial mutation assay in the absence and presence of a metabolic activation system in any of the strains tested.

 

Genetic toxicity (cytogenicity) in mammalian cells in vitro

An in vitro mammalian chromosome aberration test was conducted with N-methyl-N-[C18-(unsaturated)alkanoyl]glycine (EC 701-177-3) in accordance with OECD TG 473 under GLP conditions (LAUS, 2010). The induction of structural chromosome aberrations was evaluated in vitro in lymphocytes of fresh heparinised human whole blood cultures, incubated for 4 h with and without and for 22 h without a metabolic activation system (S9-mix from rats treated with Aroclor 1245). Concentrations of 10 - 40 µg/mL (4 h incubation) and 0.5 - 50 µg/mL (22 h incubation) of the test substance in the vehicle DMSO were applied. The negative as well as the positive controls showed the expected results. In the pre-experiment cytotoxicity was observed from 55.3 µg/mL with and without metabolic activation. In the main experiments a reduction in the mitotic index was observed from 30 µg/mL without and from 40 µg/mL with metabolic activation. No statistically or biologically significant increase in the incidence of chromosome aberrations was observed. Therefore, under the conditions of the study, the test substance did not show clastogenic activity in this chromosomal aberration test with and without metabolic activation performed in peripheral human lymphocytes in vitro.

An in vitro mammalian chromosome aberration test was conducted with Sodium N-lauroylsarcosinate (CAS 137-16-6) in accordance with OECD TG 473 under GLP conditions (Harlan, 2010a). The induction of structural chromosome aberrations was evaluated in vitro in lymphocytes of fresh heparinised human whole blood cultures, incubated for 4 and 24 h with and without a metabolic activation system (S9-mix from rats treated with phenobarbitone and beta-naphthoflavone). Concentrations of 22 - 360 µg/mL (4 h incubation) and 22.5 - 270 µg/mL (24 h incubation) of the test substance in Minimal Essential Media (MEM) were applied. The negative as well as the positive controls showed the expected results and were within the historical control data. In the preliminary toxicity test, haemolysis of the cultures was observed at 732.5 µg/mL and above in the 4 and 24 h exposure groups. In the main experiment, haemolysis was seen at the end of exposure at and above 270 µg/mL in the exposure groups. The test material did not induce a statistically significant increase in the numbers of polyploid cells at any dose level in any of the exposure groups. No statistically or biologically significant increase in the incidence of chromosome aberrations was observed. Therefore, under the conditions of the study, the test substance did not show clastogenic activity in this chromosomal aberration test with and without metabolic activation performed in peripheral human lymphocytes in vitro.

An in vitro mammalian chromosome aberration test was conducted with Sodium N-methyl-N-(1-oxotetradecyl) aminoacetate (CAS 30364-51-3) in accordance with OECD TG 473 under GLP conditions (Harlan, 2013b). The induction of structural chromosome aberrations was evaluated in vitro in lymphocytes of freshly heparinised human whole blood cultures, incubated for 4 and 24 h with and without a metabolic activation system (S9-mix from rats treated with phenobarbitone and beta-naphthoflavone). Concentrations of 12 - 200 µg/mL (4 h and 24 h incubation) of the test substance in Minimal Essential Media (MEM) with and without metabolic activation were applied. The negative as well as the positive controls showed the expected results and were within the historical control data. Haemolysis was also observed at and above 100.4 µg/mL in the two 4(20) h exposure groups and at above 200.9 µg/mL in the 24 h continuous exposure group. In the first experiment, haemolysis was seen at and above 100 µg/mL in the exposure groups in absence of metabolic activation, and at 200 µg/mL in presence of metabolic activation. The mitotic index data show that 19% mitotic inhibition and 34% mitotic inhibition was achieved at 100 µg/mL in the absence and presence of metabolic activation respectively. In the second experiment haemolysis and reduced cell pellets were observed at the end of the exposure period at 200 µg/mL in the absence of metabolic activation, and at 100 µg/mL in the presence of metabolic activation. The mitotic index data show that 63% mitotic inhibition was achieved at 75 µg/mL in the absence of metabolic activation. In the presence of metabolic activation the response was not marked with a modest 16% mitotic inhibition being observed. The test material did not induce a statistically significant increase in the numbers of polyploid cells at any dose level in any of the exposure groups. No statistically or biologically significant increase in the incidence of chromosome aberrations was observed. Therefore, under the conditions of the study, the test substance did not show clastogenic activity in this chromosomal aberration test with and without metabolic activation performed in peripheral human lymphocytes in vitro.

Genetic toxicity (mutagenicity) in mammalian cells in vitro

The in vitro mammalian cell gene mutation testing of N-methyl-N-[C18-(unsaturated)alkanoyl]glycine (EC 701-177-3) was carried out according to OECD TG 476 under GLP conditions (Harlan, 2010b). Gene mutations in the HPRT locus were investigated in Chinese hamster lung fibroblasts (V79) in the presence and absence of a metabolic activation system (Phenobarbital/beta-naphthoflavone-induced rat liver, S9). V79 cells were incubated with the test material at 0.25, 0.5, 1, 2 and 4 µg/mL for 4 h in the absence and at 4, 8, 16, 32 and 48 µg/mL in the presence of a metabolic activation system. Concentrations of the second experiment without metabolic activation for an exposure time of 24 h ranged from 4 to 96 µg/mL, and concentrations with metabolic activation for an exposure period of 4 h ranged from 4 to 56 µg/mL. The vehicle and positive controls in the study showed the expected results and were within the range of historical control data of the laboratory. Cytotoxicity was apparent at concentrations from 4 µg/mL and 48 µg/mL in experiment I without and with metabolic activation, respectively. In the second experiment, cytotoxicity was observed from 96 µg/mL and 56 µg/mL without and with metabolic activation, respectively. In the second experiment, precipitation was observed from 237.5 µg/mL after 24 h without metabolic activation. There was no significant increase in the number of forward mutations at the HPRT locus of V79 cells treated with the test material, neither in the presence nor in the absence of a metabolic activation system. Under the conditions of the study, N-methyl-N-[C18-(unsaturated)alkanoyl]glycine(EC 701-177-3) did not show gene mutation activity in this test performed in V79 cells in vitro.

The in vitro mammalian cell gene mutation study of Sodium N-lauroylsarcosinate (CAS 137-16-6) was carried out according to OECD TG 476 under GLP conditions (Harlan, 2010c). Gene mutations in the thymidine kinase locus were investigated in L5178Y mouse lymphoma cells in the presence and absence of a metabolic activation system (Phenobarbital/beta-naphthoflavone-induced rat liver, S9).In the first experiment, cells were exposed for 4 h to test substance at concentrations of 6.25-70 µg/mL and 12.5-100 µg/mL without and with metabolic activation, respectively. Concentrations of the second experiment without metabolic activation for an exposure time of 24 h ranged from 3.13 to 80 µg/mL. The vehicle and positive controls in the study showed the expected results and were within the range of historical control data of the laboratory. In the short- and long-term exposure experiments, cytotoxicity was observed from 60 and 70 µg/mL (4 h) without and with metabolic activation and from 12.5 µg/mL (24 h), respectively. There was no significant increase in the number of forward mutations at the thymidine kinase locus of L5178Y mouse lymphoma cells treated with the test material, neither in the presence nor in the absence of a metabolic activation system. Under the conditions of the study, Sodium N-lauroylsarcosinate (CAS 137-16-6) did not show gene mutation activity in this test performed in L5178Y mouse lymphoma cells in vitro.

 

The in vitro mammalian cell gene mutation study of Sodium N-methyl-N-(1-oxotetradecyl) aminoacetate (CAS 30364-51-3) was carried out according to OECD TG 476 under GLP conditions (Harlan, 2013c). Gene mutations in the thymidine kinase locus were investigated in L5178Y mouse lymphoma cells in the presence and absence of a metabolic activation system (Phenobarbital/beta-naphthoflavone-induced rat liver, S9). In the first experiment, cells were exposed for 4 h to test substance at eight concentrations of 1.25 - 50 µg/mL without and with metabolic activation. Nine concentrations of the second experiment without metabolic activation for an exposure time of 24 h ranged from 5 - 60 µg/mL. Nine concentrations of the second experiment for an exposure of 4 h ranged from 10 - 50 µg/mL in presence of metabolic activation. The vehicle and positive controls in the study showed the expected results and were within the range of historical control data of the laboratory. In the first and second experiment there was evidence of marked toxicity following exposure to the test item in both the absence and presence of metabolic activation, as indicated by the RTG and % RSG values. There was no significant increase in the number of forward mutations at the thymidine kinase locus of L5178Y mouse lymphoma cells treated with the test material, neither in the presence nor in the absence of a metabolic activation system. Under the conditions of the study, Sodium N-methyl-N-(1-oxotetradecyl) aminoacetate (CAS 30364-51-3) did not show gene mutation activity in this test performed in L5178Y mouse lymphoma cells in vitro.

Conclusion

Taken together, the available in vitro data on genetic toxicity and mutagenicity from the registered substance and several analogue substances do not indicate any mutagenic and clastogenic potential to be expected with respect to the registered substance.

Justification for classification or non-classification

The available genotoxicity and mutagenicity data from the registered substance and from analogue substances are conclusive but not sufficient for classification according to Regulation (EC) No. 1272/2008 (CLP). Therefore, applying the read-across approach, the registered substance N-(1-oxotetradecyl)sarcosine (CAS 52558-73-3) is considered not to meet the criteria for classification for genetic toxicity.