With the increasing adoption of carbon-based strategies to enhance methanogenic processes, there is a growing concern regarding the correlation between biochar properties and its stimulating effects on anaerobic digestion (AD) under ammonia inhibition. This study delves into the relevant characteristics and potential mechanisms of biochar in the context of AD system under ammonia inhibition. The introduction of optimized biochar, distinguished by rich CO bond, abundant defect density, and high electronic capacity, resulted in a significant reduction in the lag period of anaerobic digestion system under 5.0 g/L ammonia stress, approximately by around 63 % compared to the control one. Biochar helps regulate the community structure, promotes the accumulation of acetate-consuming bacteria, in the AD system under ammonia inhibition. More examinations show that biochar promotes direct interspecies electron transfer in AD system under ammonia inhibition, as evidenced by diminished levels of bound electroactive extracellular polymeric substances, increased abundance of electroactive bacteria, and notably, the up-regulation of direct interspecies electron transfer associated genes, including the conductive pili and genes, as revealed by meta-transcriptomic analysis. Additionally, gene expression related to proteins associated with ammonium detoxification were found to be up-regulated in systems supplemented with biochar. These findings provide essential evidence and insights for the selection and potential engineering of effective biochar to enhance AD performance under ammonia inhibition.

中文翻译：

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从材料和微生物角度了解生物炭在减轻厌氧消化过程中氨抑制中的作用

随着越来越多地采用碳基策略来增强产甲烷过程，人们越来越关注生物炭特性与其在氨抑制下对厌氧消化（AD）的刺激作用之间的相关性。本研究深入探讨了在氨抑制下AD系统背景下生物炭的相关特征和潜在机制。优化生物炭的引入，具有丰富的CO键、丰富的缺陷密度和高电子容量，使得厌氧消化系统在5.0 g/L氨胁迫下的滞后期显着缩短，与传统生物炭相比大约减少了63%左右。控制一.生物炭有助于调节群落结构，促进醋酸消耗菌的积累，在氨抑制下的 AD 系统中。更多的研究表明，生物炭在氨抑制下促进 AD 系统中的直接种间电子转移，这可以通过结合的电活性细胞外聚合物的水平降低、电活性细菌的丰度增加以及值得注意的是直接种间电子转移相关基因的上调来证明。包括传导菌毛和基因，如宏转录组分析所揭示的。此外，发现与铵解毒相关的蛋白质相关的基因表达在补充生物炭的系统中上调。这些发现为有效生物炭的选择和潜在工程提供了重要的证据和见解，以增强氨抑制下的 AD 性能。