Effect Mechanisms of Bisphenol A (BPA) on Aerobic Denitrification: Hierarchical Gene Suppression and Oxidative Stress

Bisphenol A (BPA), a pervasive endocrine-disrupting compound (EDC), threatens microbial nitrogen cycling, yet its mechanisms in disrupting aerobic denitrification remain poorly defined. This study elucidates the inhibitory effects of BPA on Pseudomonas stutzeri HD4-1. Dose-dependent suppression was evident: nitrate reduction rates decreased by 33%-95% at ≥ 1 mg L^-1 BPA, accompanied by nitrite accumulation (54.7-78.3 mg L^-1) and exponential N₂O emission (76.7 mg L^-1, 147-fold increase). Mechanistically, BPA induced oxidative stress (ROS: 152.6%-225.6% of control), cytomembrane damage (LDH release: 125.6%-232.1%), and metalloenzyme inactivation (N₂OR activity inhibition: 94.5%-96.4%). Concurrent transcriptional repression-notably of nosZ (2.8-9.3-fold suppression)-impaired N₂O reduction, compounded by 33%-77% declines in electron transport system activity (ETSA), exacerbating metabolic bottlenecks. Gene inhibition hierarchy (nosZ > cnorB > nirS > napA) mirrored preferential failure of terminal denitrification steps. The insight into effect mechanism of BPA on aerobic denitrification is of particular significance to provide its ecological risk assessment in aquatic ecosystems and upgrade nitrogen removal process in EDC-containing wastewater treatment plant.