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Polyethylene microplastics impose reversible redox suppression in sulfur-driven wastewater treatment systems under antibiotic co-stress
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Scientists found that tiny plastic particles (microplastics) can weaken the "helpful bacteria" wastewater treatment plants use to break down antibiotics and pollutants, causing cell stress and reducing how well antibiotics get removed from water. The good news: this damage isn't permanent—once the microplastics were removed, the bacteria bounced back and antibiotic removal returned to normal. This matters because it suggests treatment plants could recover from temporary microplastic pollution spikes, but it also shows how these tiny plastics can interfere with systems designed to keep contaminants like antibiotics out of our water supply
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.
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