Exploring the toxicity of bisphenol A and its analogue bisphenol S-MPE to Escherichia coli K12 from integrated AutoQSAR and transcriptomics analysis

Bisphenol A (BPA) analogues are a group of emerging contaminants as substitutes for BPA. Bacteria are acknowledged as indispensable parts of the ecosystem, whereas the bacterial toxicity data for BPA analogues is still lacking. Herein the wild-type and Δacriflavine resistance B (acrB) strains of E. coli K12 were exposed to BPA and bisphenol S-MPE (BPS-MPE), a BPA analogue already detected in environmental compartments but less studied yet, respectively. In comparison with the control, the growth of the wild-type strain was significantly promoted by 50 nmol L⁻¹ BPA and BPS-MPE at stationary phase, while that of the ΔacrB strain increased initially but decreased thereafter at 5 and 50 nmol L⁻¹ BPA and BPS-MPE. Therefore, lack of acrB confers a higher susceptibility to BPA and BPS-MPE. They induced hormetic effects on the expressions of acrB and Type II topoisomerases and a concentration-dependent decrease in the ATP levels. The predicted minimum inhibitory concentrations of BPA and BPS-MPE by Kernel Partial Least Squares dendritic model agree well with the measured values. Transcriptomics showed that BPA and BPS-MPE not only resulted in significant enrichment of Gene ontology terms relevant to transport, ATPase activity, binding and cell membrane, but also inhibited oxidative phosphorylation and ATP binding cassette transporters pathways. Trend analysis revealed the presence of three significant clusters, all of which showed higher changes in gene expression caused by 0.5 nmol L⁻¹ BPS-MPE compared to 0.5 nmol L⁻¹ BPA consistently. Our results unveiled BPA-like toxicity of BPS-MPE to E. coli K12 at environmentally relevant concentrations.