How halogenated aromatic compounds affect the electron supply and consumption in glucose supported denitrification?

Halogenated aromatic compounds possess bidirectional effects on denitrifying bio-electron behavior, providing electrons and potentially interfering with electron consumption. This study selected the typical 4-chlorophenol (4-CP, 0-100 mg/L) to explore its impact mechanism on glucose-supported denitrification. When COD(glucose)/COD(4-CP)=28.70-3.59, glucose metabolism remained the dominant electron supply process, although its removal efficiency decreased to 73.84-49.66 %. When COD(glucose)/COD(4-CP)=2.39-1.43, 4-CP changed microbial carbon metabolism priority by inhibiting the abundance of glucose metabolizing enzymes, gradually replacing glucose as the dominant electron donor. Moreover, 5-100 mg/L 4-CP reduced adenosine triphosphate (ATP) by 15.52-24.67 % and increased reactive oxygen species (ROS) by 31.13-63.47 %, causing severe lipid peroxidation, thus inhibiting the utilization efficiency of glucose. Activated by glucose, 4-CP dechlorination had stronger electron consumption ability than NO2--N reduction (NO3--N > 4-CP > NO2--N), combined with the decreased nirS and nirK genes abundance, resulting in NO2--N accumulation. Compared with the blank group (0 mg/L 4-CP), 5-40 mg/L and 60-100 mg/L 4-CP reduced the secretion of cytochrome c and flavin adenine dinucleotides (FAD), respectively, further decreasing the electron transfer activity of denitrification system. Micropruina, a genus that participated in denitrification based on glucose, was gradually replaced by Candidatus_Microthrix, a genus that possessed 4-CP degradation and denitrification functions after introducing 60-100 mg/L 4-CP.

Recovery mechanism of bio-promoters on Cr(VI) suppressed denitrification: Toxicity remediation and enhanced electron transmission.

Although the biotoxicity of heavy metals has been widely studied, there are few reports on the recovery strategy of the inhibited bio-system. This study proposed a combined promoter-I (Primary promoter: l-cysteine, biotin, and cytokinin + Electron-shuttle: PMo12) to recover the denitrification suppressed by Cr(VI). Compared with self-recovery, combined promoter-I shortened the recovery time of 28 cycles, and the recovered reactor possessed more stable long-term operation performance with >95 % nitrogen removal. The biomass increased by 7.07 mg VSS/(cm3 carrier) than self-recovery due to the promoted bacterial reproduction, thereby reducing the toxicity load of chromium per unit biomass. The combined promoter-I strengthened the toxicity remediation by promoting 92.84 % of the intracellular chromium release and rapidly activating anti-oxidative stress response. During toxicity remediation, ROS content quickly decreased, and the PN/PS value was 2.27 times that of self-recovery. PMo12 relieved Cr(VI) inhibition on NO3--N reduction by increasing NAR activity. The enhanced intracellular and intercellular electron transmission benefited from the stimulated NADH, FMN, and Cyt.c secretion by the primary promoter and the improved transmembrane electron transmission by Mo. PMo12 and the primary promoter synergized in regulating community structure and improving microbial richness. This study provided practical approaches for microbial toxicity remediation and maintaining high-efficiency denitrification.