A comparative study based on the genotoxicity of 9-aminoacridine (9-AA) and 8-methoxypsoralen (8-MOP) transpired using a lux biosensor E. coli MG1655 (pColD-lux), having a recombinant plasmid with a lux operon under a gene promoter colD. The colD (cda) gene is part of the E. coli SOS regulon that also ensures DNA repair and cell resistance to DNA damage. The Gen colD (cda) includes SOS-regulon E. coli. The lux operon performs a reporter function characterizing the SOS response to DNA damage. The considered genotoxicity of 9-AA and activated UVA (λ = 365 nm) 8-MOP came from manipulating the luminescence intensity of the biosensor. The 8-MOP induction in bacteria of the SOS response depended on concentrations of UVA and 8-MOP. With higher doses of UVA, a 25-fold decrease emerged in the survival of bacterial cells (from 2х10⁸ to 8х10⁶ КОЕ), while an increase in the intensity of the SOS response by 675 times for 10⁶ cells was evident in viable cells. The DNA-damaging and lethal effect of 8-MOP in bacteria relied on the concentrations of UVA and 8-MOP.

Keywords: 9-aminoacridine, 8-methoxypsoralen, lux-biosensor, E. coli, gene promoter ColD, SOS response, UV irradiation, monoadducts, diadducts

Key findings: A comparative study of the genotoxicity of 9-aminoacridine (9-AA) and UVA-activated 8-methoxypsoralen (8-MOP) using a lux biosensor in E. coli MG1655 (pColD-lux) showed a considerable enhancement in the SOS response. Exposure to the highest concentrations of UVA and 8-MOP resulted in a 25-fold decrease in bacterial survival and a 675-fold increase in SOS response intensity in viable cells, with DNA damaging based on their concentrations.