...
首页> 外文期刊>The Science of the Total Environment >Metagenomic insights into aniline effects on microbial community and biological sulfate reduction pathways during anaerobic treatment of high-sulfate wastewater
【24h】

Metagenomic insights into aniline effects on microbial community and biological sulfate reduction pathways during anaerobic treatment of high-sulfate wastewater

机译:高硫酸盐废水的厌氧处理过程中苯胺患者对微生物群落和生物硫酸盐降低途径的苯胺态洞察

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

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 biore-actor 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.
机译:为了综合了解硫酸盐降低途径的变化,应对毒性应激和微生物群落的变化和硫酸盐减少的性能,建立了一种实验室扩增的颗粒污泥床反应器(EGSB),处理高硫酸苯胺浓度的高硫酸盐废水从0到480mg / L的高通量测序和偏见方法被应用于通过分类和功能性谱系破译苯胺胁迫下的硫酸盐降低的分子机制。厌氧系统中的苯胺增加诱导挥发性脂肪酸(VFA)的积累,进一步将生物效应器转化为酸化,这是系统性能恶化的主要原因,最终导致有毒游离硫化物的积累。此外,苯胺引发了与硫酸盐还原途径有关的细菌群落和基因的变化。苯胺的增加从0到320 mg / L富集的总硫酸盐还原细菌(SRB),以及最丰富的属植物是脱硫纤维素,占总SRB的66.85-91.25%。当苯胺超过160mg / L时,显然抑制了同化硫酸盐还原途径,而与硫酸化硫酸盐还原途径相关的基因均显示出苯胺含量增加的向上趋势。与硫酸化硫酸盐还原途径相关的厌氧抗性SRB(例如脱硫胶质升)的富集也证实了硫酸盐降低在高苯胺条件下变化的潜在机制。总之,这些结果全面为苯胺对处理高硫酸盐废水的生物硫酸盐还原方法和潜在的分子机制的影响,这些结果全面提供了苯胺的影响,这可能突出SRB和相关硫酸盐还原基因在处理过程中的重要作用。

著录项

  • 来源
    《The Science of the Total Environment》 |2020年第10期|140537.1-140537.11|共11页
  • 作者单位

    State Key Laboratory of Pollution Control and Resources Reuse School of the Environment Nanjing University Nanjing 210023 China;

    State Key Laboratory of Pollution Control and Resources Reuse School of the Environment Nanjing University Nanjing 210023 China;

    Department of Civil and Environmental Engineering University of California Los Angeles CA 90095 United States;

    State Key Laboratory of Pollution Control and Resources Reuse School of the Environment Nanjing University Nanjing 210023 China;

    State Key Laboratory of Pharmaceutical Biotechnology School of Life Sciences Nanjing University Nanjing 210023 China;

    State Key Laboratory of Pharmaceutical Biotechnology School of Life Sciences Nanjing University Nanjing 210023 China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    Aniline; Dissimilation; Microbial community; Reduction pathways; Functional genes; Metagenomic analyses;

    机译:苯胺;异化;微生物群落;减少途径;功能基因;Metagenomic分析;

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号