利用宏基因组学分析壬基酚对剩余污泥厌氧发酵产酸的影响

Effect of Nonylphenol on Anaerobic Fermentation of Waste Activated Sludge for Short-chain Fatty Acids Production Based on Metagenomic Analysis

摘要:

研究了环境雌激素壬基酚（NP）对剩余污泥厌氧发酵产酸的影响，并利用宏基因组测序手段分析影响机制。NP促进污泥厌氧发酵产酸，随NP含量的提高，该促进作用呈先增加后减少的趋势。当NP含量为200 mg·kg^-1干污泥时，污泥发酵产生的短链脂肪酸（SCFAs）达最大值，为空白组SCFAs产量的2倍，乙酸产量为空白组的3倍。基于宏基因组学的机理研究表明，NP导致不利于SCFAs积累的耗酸微生物有所削减，产酸微生物大量积累。NP存在时，以葡萄糖为底物的糖酵解、以氨基酸为底物的脱氨基和以脂肪酸为底物的β氧化过程功能基因相对丰度提高；单糖和氨基酸等有机底物由胞外向胞内运输的腺苷三磷酸结合盒转运蛋白、运输至胞内的有机底物向SCFAs代谢转化的双组分系统及胞内产生的SCFAs外排转运蛋白的相关功能基因丰度大幅提高。最后，NP引起了与细胞生长和保护机制密切相关的群体感应调控的生物膜合成基因丰度显著提升。

Abstract:

The effect of environmental estrogen nonylphenol （NP） on the anaerobic fermentation of waste activated sludge for short-chain fatty acids （SCFAs） production was investigated， and the mechanism was revealed by means of metagenomic sequencing. It was found that NP promoted the SCFAs production during the anaerobic fermentation of the sludge， and the acceleration increased firstly and then decreased with the increase of NP concentration. The yield of SCFAs reached the maximum when the content of NP was 200 mg·kg^-1 dry sludge， which was 2-fold of that in the control. The production of acetic acid was increased by almost three times due to the presence of NP. Mechanism exploration based on metagenomic analysis exhibited that the reduction of acid-consuming and the improvements of acidogenic microorganisms was advantageous to the accumulation of SCFAs with NP. In addition， the relative abundance of functional genes in glycolysis， deamination and β-oxidation of glucose， amino acid and fatty acid was improved obviously. Also， the abundance of genes in adenosine triphosphate binding box transporters （ABC transporters） which control the transport of organic substrates into cells， two-component system for the SCFAs metabolism， and ABC transporters on SCFAs efflux increased remarkably. Furthermore， the abundance of genes related to biofilm formation regulated by quorum sensing in the presence of NP was increased， which was beneficial to cell growth and defense.