Abstract

This study explored the response of NO3--N bioreduction to Cr(VI) stress, including reduction efficiency and the pathways involved (denitrification and dissimilatory nitrate reduction to ammonium (DNRA)). Different response patterns of NO3--N conversion were proposed under Cr(VI) suppress (0, 0.5, 5, 15, 30, 50, and 80 mg/L) by evaluating Cr(VI) dose dependence, toxicity accumulation, bioelectron behavior, and microbial community structure. Cr(VI) concentrations of >30 mg/L rapidly inhibited NO3--N removal and immediately induced DNRA. However, denitrification completely dominated the NO3--N reduction pathway at Cr(VI) concentrations of <15 mg/L. Therefore, 30 and 80 mg/L Cr(VI) (R4 and R6) were selected to explore the selection of the different NO3--N removal pathways. The pathway of NO3--N reduction at 30 mg/L Cr(VI) exhibited continuous adaptation, wherein the coexistence of denitrification (51.7%) and DNRA (13.6%) was achieved by regulating the distribution of denitrifiers (37.6%) and DNRA bacteria (32.8%). Comparatively, DNRA gradually replaced denitrification at 80 mg/L Cr(VI). The intracellular Cr(III) accumulation in R6 was 6.60-fold greater than in R4, causing more severe oxidant injury and cell death. The activated NO3--N reduction pathway depended on the value of nitrite reductase activity/nitrate reductase activity, with 0.84-1.08 associated with DNRA activation and 1.48-1.57 with DNRA predominance. Although Cr(VI) increased microbial community richness and improved community structure stability, the inhibition or death of nitrogen-reducing microorganisms caused by Cr(VI) decreased NO3--N reduction efficiency.

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