Abstract

Here, the toxicity responses mechanism of the simultaneous partial nitritation, anammox and denitrification (SNAD) system to Zn(II) exposure were explored with emphasis on the repressed quorum sensing (QS) regulation on extracellular electron transfer and microbial metabolism. Results showed that Zn(II) accumulated in cells and induced oxidative stress, which led to microbial structure destruction. The increased electron transfer impedance and reduced redox substances (flavin/Cytochrome c) implied that Zn(II) affected electron transfer. The decreased ATP level, dehydrogenase and nitrogen related enzymatic activities showed Zn(II) affected organic matter and nitrogen metabolism. Furthermore, combined with Pearson network analysis, Zn(II) exposure disturbed the QS to decrease Acyl Homoserine Lactones (AHLs) secretion responsible for regulating extracellular electron transfer and microbial metabolism, thereby disturbing the performance of the SNAD system. This study provided new insights into the toxicity responses mechanism of the SNAD system to HM exposure.

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