The roles of membrane permeability and efflux pumps in the toxicity of bisphenol S analogues (2,4-bisphenol S and bis-(3-allyl-4-hydroxyphenyl) sulfone) to Escherichia coli K12

Abstract

Bisphenol S (BPS) analogues are a group of recently reported emerging contaminants in the environment. Bacteria are important components of food webs. However, the potential risks of BPS analogues in bacteria have not been fully addressed. The toxicity effects and related mechanisms of two BPS analogues with different molecular weights (2,4-bisphenol S (2,4-BPS) and bis-(3-allyl-4-hydroxyphenyl) sulfone (TGSA)) on Escherichia coli K12 were compared. The minimum inhibitory concentration (MIC) of 2,4-BPS in the wild-type of E. coli K12 was lower than that of TGSA. The membrane permeability of the wild-type increased significantly after exposed to the same concentrations (0.5–50 nmol L−1) of 2,4-BPS and TGSA. In addition, 2,4-BPS induced more significant changes in membrane permeability than TGSA. Hormetic effects of 2,4-BPS and TGSA in the wild-type strain were noted in the levels of outer membrane proteins (ompC and ompF), multidrug efflux pump acriflavine resistance B (acrB) and type II topoisomerases. Transcriptomic results indicated these two BPS analogues inhibited the function of ABC transporters. In contrast to TGSA, 2,4-BPS affected DNA replication, tricarboxylic acid cycle, oxidative phosphorylation, and inhibited energy metabolism. Compared with wild-type strain, the ΔacrB mutant strain showed enhanced susceptibility to 2,4-BPS and TGSA with their MICs reduced by 20% and 11%, respectively. Deletion of the acrB affected the growth characteristics and induced stronger oxidative stress than the wild-type strain when exposed to 2,4-BPS or TGSA. The results suggested that 2,4-BPS were more toxic to E. coli K12 than TGSA in the concentration range of 0.5–50 nmol L−1, which was supported by the evidence from their impacts on membrane permeability and efflux pumps.