期刊
ENVIRONMENTAL CHEMISTRY LETTERS
卷 20, 期 3, 页码 1553-1560出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s10311-022-01397-x
关键词
Bisphenol contaminants; Antibiotic resistance genes; Conjugative transfer; Microbial risks
资金
- Singapore-China Joint Research Grant Call (NRF-NSFC 3rd Joint Grant Call-Earth Science) [41861144023]
- Natural Science Foundation of China-Joint Fund Project [U2005206]
- Xiamen Municipal Bureau of Science and Technology [YDZX20203502000003]
This study demonstrates that bisphenol S and bisphenol AF can accelerate the spread of antibiotic resistance genes between bacteria, which may have implications for the dissemination of antibiotic resistance in the environment and in gut microbial communities of wildlife and human.
The global dissemination of antibiotic resistance is severely threatening public health. Several non-antibiotic chemicals facilitate the horizontal transfer of antibiotic resistance genes. Bisphenol analogs, e.g., bisphenol S and bisphenol AF, are known pollutants, yet their effects on the propagation and spread of antibiotic resistance genes remain unknown. Our study demonstrates for the first time that bisphenol S and bisphenol AF at environmentally relevant concentrations of 0.1-100.0 mu g/L accelerates 2-5 folds the conjugative transfer frequency of RP4 plasmid-borne antibiotic resistance genes within and across bacterial genera, from Escherichia coli DH5 alpha to Escherichia coli HB101 or Salmonella enterica. Bisphenol S and bisphenol AF exerted no effect on the bacterial growth and little change in cell membrane permeability. Accelerated conjugative transfer is explained by the repression of the global regulator, with a maximum relative expression level of 0.23, and of the vertical transfer system (0.26), with simultaneous up-regulation of DNA horizontal transfer and replication system (3.66). This bisphenols-induced conjugative transfer of antibiotic resistance genes could promote the spread of antibiotic resistance in the environment and in gut microbial communities of wildlife and human.
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