Sulfamethoxazole forces a survival-first metabolic switch in sludge-free phosphate bioreduction
This study investigates the mechanistic response of a sludge-free phosphate bioreduction system to short-term sulfamethoxazole (SMX) stress (0-200 ug/L). SMX induced a dose-dependent decline in performance, with PO4^3--P removal dropping from 86.67% to 56.57%, COD removal from 97.83% to 38.80%, and phosphine production from 9.30 to 3.42 ug/(L h). Mechanistically, SMX triggered a "survival-first" metabolic switch, redirecting carbon and reducing equivalents toward extracellular polymeric substance (EPS) synthesis, evidenced by a PN/PS ratio increase from 0.22 to 0.82. This defensive adaptation came at the expense of energy metabolism, as indicated by decreased ATP levels and electron transport system activity (ETSA), alongside disrupted electron flux from cytochrome C leakage and increased membrane permeability. Electrochemical analysis confirmed impaired extracellular electron transfer and heightened interfacial resistance. Concurrently, SMX reshaped the microbial community, driving a shift from a high-diversity functional balance to a low-diversity, tolerant structure (e.g., Pseudomonadota decline, Cyanobacteriota enrichment). These findings reveal that SMX forces a multi-cascade collapse of phosphate bioreduction, centered on electron transport chain disruption, providing a theoretical basis for evaluating this novel process under antibiotic co-contamination.