The role of nucleotide excision repair on 2,6- and 3,5-dimethylaniline-induced genotoxicity
J Environ Biol
;
2020 Mar; 41(2): 216-221
Article
| IMSEAR
| ID: sea-214496
ABSTRACT
Aim:
To examine the possible role of nucleotide excision repair (NER) in affecting the ultimate mutagenic potency of 2,6- and 3,5-dimethylaniline (DMA) and their metabolites.Methodology:
Two cell lines, nucleotide excision repair (NER)-proficient AA8 and deficient UV5 cells were treated with 50, 100, 250, 500 and 1000 μM of 2,6- and 3,5-DMA for 48 hr or their N-hydroxyl and aminophenol metabolites for 1 hr. Cell survival was determined by trypan blue exclusion assay, and 8-azaadenine-resistant mutants at adenine phosphoribosyltransferase (aprt) gene locus were evaluated.Results:
A dose-dependent increase in cytotoxicity and mutant fraction was observed in AA8 and UV5 cells, treated with 2,6- and 3,5-DMA and their metabolites, but showed considerable variation in potency; N-hydroxyl and aminophenol metabolites of 2,6- and 3,5-DMA in serum-free α-minimal essential medium (MEM) having the highest potency, and 2,6- and 3,5-DMA in regular MEM at least. Repair-deficient UV5 cells were more sensitive to cytotoxic and mutagenic action than repair-proficient AA8 cells.Interpretation:
These findings suggest that 2,6- and 3,5-DMA-induced DNA damage response may trigger cytotoxicity and mutagenicity when not completely repaired
Full text:
Available
Index:
IMSEAR (South-East Asia)
Journal:
J Environ Biol
Year:
2020
Type:
Article
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