The unexpected role of aged microplastics in inhibiting antibiotic resistance gene spread

Microplastics (MPs) are known to promote the spread of antibiotic resistance genes (ARGs) through biofilm formation, pollutant co-selection, and enhanced horizontal gene transfer (HGT). However, emerging evidence suggests that aged microplastics (A-MPs) may, under certain conditions, exert inhibitory effects via two coupled mechanisms: radical-mediated suppression of cellular and extracellular DNA, and plasmid-level interference with replication and transfer. Photo-oxidative aging introduces oxygen-containing functional groups and enables the surface generation of environmentally persistent free radicals (EPFRs) and reactive oxygen species (ROS), especially hydroxyl radicals (•OH). These reactive intermediates can damage cell membranes, inhibit biofilm formation, and fragment extracellular DNA, reducing conjugation and transformation frequencies. Meanwhile, nanoscale or highly concentrated A-MPs can suppress plasmid replication, particularly of low-copy plasmids, and hinder donor. recipient contact through aggregation and spatial hindrance, thereby decreasing HGT efficiency. A concentration–size–replication relationship reconciles the duality of observed effects: smaller or low-dose MPs may transiently enhance permeability and uptake, whereas higher radical fluxes and aggregation shift systems toward inhibition. This review consolidates current evidence and proposes that the oxidative microenvironments associated with aged microplastics may indirectly constrain ARG dissemination, providing a new hypothesis and research direction for understanding their ecological role in antibiotic resistance dynamics.