For comprehensive insights into the change of sulfate reduction pathway responding to the toxic stress and the shift of microbial community and performance of sulfate reduction, we built a laboratory-scale expanded granular sludge bed reactor (EGSB) treating high-sulfate wastewater with elevated aniline concentrations from 0 to 480 mg/L. High-throughput sequencing and metagenomic approaches were applied to decipher the molecular mechanisms of sulfate reduction under aniline stress through taxonomic and functional profiles. The increasing aniline in the anaerobic system induced the accumulation of volatile fatty acids (VFA), further turned the bioreactor into acidification, which was the principal reason for the deterioration of system performance and finally resulted in the accumulation of toxic free sulfide. Moreover, aniline triggered the change of bacterial community and genes relating to sulfate reduction pathways. The increase of aniline from 0 to 320 mg/L enriched total sulfate-reducing bacteria (SRB), and the most abundant genus was Desulfomicrobium, accounting for 66.85–91.25% of total SRB. The assimilatory sulfate reduction pathway was obviously inhibited when aniline was over 160 mg/L, while genes associated with dissimilatory sulfate reduction pathways all exhibited an upward tendency with the increasing aniline content. The enrichment of aniline-resistant SRB (e.g. Desulfomicrobium) carrying genes associated with the dissimilatory sulfate reduction pathway also confirmed the underlying mechanism that sulfate reduction turned into dissimilation under high aniline condition. Taken together, these results comprehensively provided solid evidence for the effects of aniline on the biological sulfate reduction processes treating high-sulfate wastewater and the underlying molecular mechanisms which may highlight the important roles of SRB and related sulfate reduction genes during treatment.

为了全面了解硫酸盐还原途径对毒性胁迫的响应以及微生物群落的变化和硫酸盐还原性能的变化，我们建立了实验室规模的膨胀式颗粒污泥床反应器（EGSB），用于处理苯胺浓度较高的高硫酸盐废水。 0至480 mg / L。应用高通量测序和宏基因组学方法，通过分类学和功能谱分析了苯胺胁迫下硫酸盐还原的分子机制。厌氧系统中苯胺的增加引起挥发性脂肪酸（VFA）的积累，使生物反应器进一步酸化，这是导致系统性能下降的主要原因，并最终导致有毒游离硫化物的积累。此外，苯胺触发了细菌群落和与硫酸盐还原途径有关的基因的变化。苯胺从0增加到320 mg / L富集了总硫酸盐还原菌（SRB），并且最丰富的属是脱硫微生物，占总SRB的66.85–91.25％。当苯胺含量超过160 mg / L时，同化硫酸盐还原途径明显受到抑制，而与异化硫酸盐还原途径相关的基因均随着苯胺含量的增加而呈上升趋势。苯胺抗性SRB（例如脱硫微生物）的富集）携带与异化硫酸盐还原途径相关的基因也证实了在高苯胺条件下硫酸盐还原变成异化的潜在机理。综上所述，这些结果为苯胺对处理高硫酸盐废水的生物硫酸盐还原过程的影响及其潜在的分子机理提供了有力的证据，这些分子机理可能突出了SRB和相关硫酸盐还原基因在处理过程中的重要作用。