Polyethylene microplastics impose reversible redox suppression in sulfur-driven wastewater treatment systems under antibiotic co-stress.

Microplastics and antibiotics frequently co-occur in wastewater treatment systems, yet their combined effect on sulfur-driven bioprocesses and the subsequent post-stress recovery remains poorly resolved. In this study, the long-term response of a sulfate-reducing bacteria (SRB) sludge system treating sulfamethoxazole (SMX)-laden wastewater to polyethylene microplastics (PE MPs; 100 - 800 particles/L) was investigated by combining parallel continuous-flow reactors, batch physiological assays, and metagenomic analysis. PE MPs exerted a concentration-dependent but function-differentiated inhibition, in which SMX removal was more sensitive than chemical oxygen demand (COD) removal and sulfate reduction. At 800 particles/L, SMX removal declined from 37.1 ± 4.1% to 30.5 ± 5.2%, accompanied by elevated intracellular reactive oxygen species (ROS; 138.2 ± 4.0%), increased lactate dehydrogenase (LDH) leakage (122.0 ± 7.1% of the control), weakened antioxidant capacity, and a higher dead-cell fraction (29.7 ± 2.0%). Metagenomic analysis further revealed suppression of central carbon metabolism, dissimilatory sulfate reduction, lipid metabolism, and antioxidant defense, indicating that PE MPs disrupted redox homeostasis and thereby constrained energy supply, sulfur-related electron transfer, membrane maintenance, and stress-response capacity. Notably, after PE MPs withdrawal, SMX removal recovered to 37.8 ± 4.0%, and ROS declined to 107.8 ± 2.8% despite continued SMX loading, together with partial restoration of sulfur-related functional potential. These findings support a reversible, redox-mediated metabolic suppression model rather than irreversible functional collapse, providing an engineering basis for the stable application and functional resilience evaluation of sulfur-driven biotechnologies under fluctuating microplastic exposure, while highlighting the need for future enzyme-level verification of ROS-dependent causal mechanisms.