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Size- and surface charge-dependent hormetic effects of microplastics on bacterial resistance and their interactive effects with quinolone antibiotic
Summary
This study found that polystyrene microplastics — even at low concentrations — can boost bacterial mutation rates and the frequency of antibiotic-resistance gene transfer between bacteria, with the strongest effects from positively charged, 0.1-micron particles. When microplastics and the antibiotic norfloxacin were present together, the combined risk of resistance development was greater than either alone. This raises concern that microplastic-contaminated environments may be accelerating the spread of antibiotic resistance, a major threat to human and animal health.
The facilitation of microplastics (MPs) on bacterial resistance has attracted wide concern, due to the widespread presence of MPs in environmental media and their ubiquitous contact with bacteria strains. Furthermore, MPs possibly co-exist with antibiotics to trigger combined stress on bacterial survival. Therefore, it is significant to reveal the dose-responses of MPs and MP-antibiotic mixtures on bacterial endogenous and exogenous resistance. In this study, 0.1 and 5 μm polystyrenes with no surface functionalization (PS-NF, no charge), surface functionalized with amino groups (PS-NH, positive charge) and carboxyl groups (PS-COOH, negative charge) were selected as the test MPs, and norfloxacin (NOR) was set as the representative of antibiotics. It was found that six types of PS all inhibited the growth of Escherichia coli (E. coli) but induced hormetic dose-responses on the mutation frequency (MF) and conjugative transfer frequency (CTF) of RP4 plasmid in E. coli. Moreover, these hormetic effects exhibited size- and surface charge-dependent features, where 0.1 μm PS-NH (100 mg/L) triggered the maximum stimulatory rates on MF (363.63 %) and CTF (74.80 %). The hormetic phenomena of MF and CTF were also observed in the treatments of PS-NOR mixtures, which varied with the particle size and surface charge of PS. In addition, the interactive effects between PS and NOR indicated that the co-existence of PS and NOR might trigger greater resistance risk than the single pollutants. Mechanistic exploration demonstrated that the increase of cellular reactive oxygen species and the variation of cell membrane permeability participated in the hormetic effects of PS and PS-NOR mixtures on bacterial resistance. This study provides new insights into the individual effects of MPs and the combined effects of MP-antibiotic mixtures on bacterial resistance, which will promote the development of environmental risk assessment of MPs from the perspective of bacterial resistance.
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