Microorganisms colonizing the surfaces of microplastics form a plastisphere in the environment, which captures miscellaneous substances. The plastisphere, owning to its inherently complex nature, may serve as a "Petri dish" for the development and dissemination of antibiotic resistance genes (ARGs), adding a layer of complexity in tackling the global challenge of both microplastics and ARGs. Increasing studies have drawn insights into the extent to which the proliferation of ARGs occurred in the presence of micro/nanoplastics, thereby increasing antimicrobial resistance (AMR). However, a comprehensive review is still lacking in consideration of the current increasingly scattered research focus and results. This review focuses on the spread of ARGs mediated by microplastics, especially on the challenges and perspectives on determining the contribution of microplastics to AMR. The plastisphere accumulates biotic and abiotic materials on the persistent surfaces, which, in turn, offers a preferred environment for gene exchange within and across the boundary of the plastisphere. Microplastics breaking down to smaller sizes, such as nanoscale, can possibly promote the horizontal gene transfer of ARGs as environmental stressors by inducing the overgeneration of reactive oxygen species. Additionally, we also discussed methods, especially quantitatively comparing ARG profiles among different environmental samples in this emerging field and the challenges that multidimensional parameters are in great necessity to systematically determine the antimicrobial dissemination risk in the plastisphere. Finally, based on the biological sequencing data, we offered a framework to assess the AMR risks of micro/nanoplastics and biocolonizable microparticles that leverage multidimensional AMR-associated messages, including the ARGs' abundance, mobility, and potential acquisition by pathogens.
Rising levels of antibiotic resistance are undermining ecological and human health as a result of the indiscriminate usage of antibiotics. Various resistance mechanisms have been characterized—for example, genes encoding proteins that degrade antibiotics—and yet, this requires further exploration.
Sustainable
nitrogen cycle is an essential biogeochemical
process
that ensures ecosystem safety and byproduct greenhouse gas nitrous
oxide reduction. Antimicrobials are always co-occurring with anthropogenic
reactive nitrogen sources. However, their impacts on the ecological
safety of microbial nitrogen cycle remain poorly understood. Here,
a denitrifying bacterial strain Paracoccus denitrificans PD1222 was exposed to a widespread broad-spectrum antimicrobial
triclocarban (TCC) at environmental concentrations. The denitrification
was hindered by TCC at 25 μg L–1 and was completely
inhibited once the TCC concentration exceeded 50 μg L–1. Importantly, the accumulation of N2O at 25 μg
L–1 of TCC was 813 times as much as the control
group without TCC, which attributed to the significantly downregulated
expression of nitrous oxide reductase and the genes related to electron
transfer, iron, and sulfur metabolism under TCC stress. Interestingly,
combining TCC-degrading denitrifying Ochrobactrum sp. TCC-2 with strain PD1222 promoted the denitrification process
and mitigated N2O emission by 2 orders of magnitude. We
further consolidated the importance of complementary detoxification
by introducing a TCC-hydrolyzing amidase gene tccA from strain TCC-2 into strain PD1222, which successfully protected
strain PD1222 against the TCC stress. This study highlights an important
link between TCC detoxification and sustainable denitrification and
suggests a necessity to assess the ecological risks of antimicrobials
in the context of climate change and ecosystem safety.
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