Fe(Ⅱ)-mediated detoxification mitigates low-dose rare earth elements-induced stress on anammox consortia for mining tailwater treatment.

Rare earth mining activities cause severe nitrogen pollution in watersheds, yet the residual hazardous rare earth elements (REEs) toxicity in tailings wastewater challenges biological nitrogen removal technology. This work demonstrated that introducing low-dose Fe(II) into partial denitrification/anammox (PD/A) system significantly alleviated REEs-induced stress on anammox consortia via detoxification and physical barrier reinforcement. The PD/A bioreactor with 15 mg/L Fe(II) (R1) was compared against a control without Fe(II) for real rare earth tailings wastewater treatment. Metagenomic analysis identified 1.14-fold upregulation of hydrazine (N2H4) dehydrogenase alongside substantial 5.82-fold downregulation of N2H4 synthase in R1, indicating a critical metabolic reconfiguration that expedited the degradation of toxic intermediates and alleviated REEs-mediated cytotoxicity. Electrons with lower redox potential released from N2H4 oxidation were more effectively utilized for carbon fixation, as evidenced by the upregulated electron transport complexes and Wood-Ljungdahl pathway. Concurrent biosynthetic modulation stimulated lipopolysaccharide production (module M00063) and carbohydrate storage (module M00064), collectively reinforcing microbial stress resilience through both defensive metabolites (lipopolysaccharides and trehalose) and hydrophobicity-driven aggregation. Moreover, modified 2-P logistic modeling confirmed elevated REEs inhibition thresholds under Fe(II) mediation. This study reveals the defense mechanism of Fe(II)-enhanced anammox consortia against REEs stress, providing new insights for sustainable bioremediation in rare earth mining areas.