N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG); Positive controls 2 5 WP2; 10 g/plate g/plate E. coli –TA100; – TA1535 (without metabolic activation) – 2-nitro-fluorene (2-NF) 2 TA 98; g/plate – 5 1538, (without g/plate –TA metabolic activation) 9-aminoacridine (9-AA): 50 TA1537 g/plate – (without metabolic activation) 2-aminoanthracene (2-AA): 5 g/plate - TA100, TA98, TA1538; 20 TA1535, TA1537; g/plate – 40 WP2 (with g/plate – E. coli activation) toxic effects occurred in the absence of metabolic Comment: activation for the highest dose used for all strains; a substantial increase in the number of revertant colonies with an indication of clear dose response occurred for strains TA100 (500-5000 g/plate), TA1535 (1000-5000 g/plate) and WP2 E. Coli (5000 in the presence of metabolic g/plate) activation the positive controls produced clear positive results indicating that the test system responded appropriately the test material was weakly mutagenic in the Result: bacterial strains which detect base substitution (TA100, TA1535 and WP2) in the presence of metabolic activation provided by rat liver S9 fraction Analogue Genotoxicity Results Positive evidence of genotoxicity for the analogue compound TGIC was in a number of studies quoted in the summary of TGIC toxicity provided by the notifier (National Occupational Health and Safety Commission, 1994c). A TGIC Ames test showed it to be a weak mutagen to TA98 and TA100 in the presence and absence of metabolic activation. It was also found to be mutagenic in a mouse lymphoma cell forward mutation assay both in the presence and absence of metabolic activation. It was also found to be damaging to DNA as measured by induction of unscheduled DNA synthesis in rat hepatocytes although it was negative in a similar test using human fibroblasts. in vitro,
Positive controls N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG); 2 g/plate –TA100; 5 g/plate – E. coli WP2; 10 – TA1535 (without metabolic activation) 2-nitro-fluorene (2-NF) 2 g/plate – TA 98; 5 g/plate –TA 1538, (without metabolic activation) 9-aminoacridine (9-AA): 50 g/plate – TA1537 (without metabolic activation) 2-aminoanthracene (2-AA): 5 g/plate - TA100, TA98, TA1538; 20 g/plate – TA1535, TA1537; 40 g/plate – E. coli WP2 (with activation) Comment: toxic effects occurred in the absence of metabolic activation for the highest dose used for all strains; a substantial increase in the number of revertant colonies with an indication of clear dose response occurred for strains TA100 (500-5000 g/plate), TA1535 (1000-5000 g/plate) and E. Coli WP2 (5000 g/plate) in the presence of metabolic activation the positive controls produced clear positive results indicating that the test system responded appropriately Result: the test material was weakly mutagenic in the bacterial strains which detect base substitution (TA100, TA1535 and WP2) in the presence of metabolic activation provided by rat liver S9 fraction Analogue Genotoxicity Results Positive evidence of genotoxicity for the analogue compound TGIC was in a number of studies quoted in the summary of TGIC toxicity provided by the notifier (National Occupational Health and Safety Commission, 1994c). A TGIC Ames test showed it to be a weak mutagen to TA98 and TA100 in the presence and absence of metabolic activation. It was also found to be mutagenic in a mouse lymphoma cell forward mutation assay both in the presence and absence of metabolic activation. It was also found to be damaging to DNA as measured by induction of unscheduled DNA synthesis in rat hepatocytes in vitro, although it was negative in a similar test using human fibroblasts.
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