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Journal of Environmental Biology

pISSN: 0254-8704 ; eISSN: 2394-0379 ; CODEN: JEBIDP

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    Abstract - Issue Mar 2020, 41 (2)                                     Back

nstantaneous and historical temperature effects on a-pinene

The role of nucleotide excision repair on 2,6- and 3,5-dimethylaniline-induced genotoxicity


M.Y. Kim* 

Toxicology Laboratory, Faculty of Biotechnology (Biomaterials), College of Applied Life Science, SARI, Jeju National University, Jeju, 63243, Republic of Korea

*Corresponding Author Email :

Paper received: 07.09.2019??????? ?????????????????????????????????????? Revised received: 11.12.2019????????????? ???????????????????????? Accepted: 13.01.2020



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.? ???

Key words: Dimethylaniline, Genotoxicity, Mutagenicity, Nucleotide excision repair




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