Vivianite, a notable secondary mineral formed through dissimilatory iron reduction (DIR), demonstrates great potential in addressing both eutrophication and phosphorus deficiency. However, the presence of competition for electrons from the methanogenic pathway and the low rates of Fe(III) reduction limit the creation of vivianite. In this research, H₂ was utilized as electron donor assisted by activated carbon (AC) to promote Fe(Ⅲ) reduction with FePO₄ as electron acceptors. The introduction of H₂ and H₂/AC increased the Fe(III) reduction by 23.8 % and 34.3 %, respectively. Both also increase the rate of vivianite formation. H₂ acted as an electron donor to promote Fe(III) reduction by both direct Fe(III) reduction and homoacetogenesis-acetate reduction pathways. It also suppressed the process of methanogenesis to avoid extra consumption of electrons. AC increased the rate of electron transfer, increased hydrogenase and homoacetogenesis-related enzyme activities, and enriched more Dissimilatory iron reduction bacteria (DIRB). H₂ promoted the up-regulation of Wood-Ljungdahl pathway, TCA cycle and electron transport chain related genes. AC enhanced H₂ capture and functioned as an electron shuttle. These results offer fresh perspectives on promoting Fe(III) reduction to facilitate vivianite formation.

中文翻译：

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在活性炭的辅助下，使用外源性 H2 增强污泥发酵中 Fe（III） 的还原，以形成 vivianite


Vivianite 是一种通过异化铁还原 （DIR） 形成的显着次生矿物，在解决富营养化和磷缺乏方面显示出巨大潜力。然而，来自产甲烷途径的电子竞争的存在和 Fe（III） 的低还原速率限制了 vivianite 的产生。在这项研究中，利用 H₂ 作为电子供体，在活性炭 （AC） 的辅助下促进 Fe（III.） 还原，FePO₄ 作为电子受体。H₂ 和 H₂/AC 的引入使 Fe（III） 减少分别增加了 23.8 % 和 34.3 %。两者都增加了 vivianite 的形成速度。H₂ 作为电子供体，通过直接 Fe（III） 还原和同源乙酸乙酸还原途径促进 Fe（III） 还原。它还抑制了甲烷生成过程，以避免额外消耗电子。AC 提高了电子转移速率，增加了氢化酶和同源乙酸生成相关酶活性，并富集了更多的异化性铁还原菌 （DIRB）。H₂ 促进 Wood-Ljungdahl 通路、TCA 循环和电子传递链相关基因的上调。AC 增强了 H₂ 捕获并起到电子穿梭的作用。这些结果为促进 Fe（III） 还原以促进 vivianite 的形成提供了新的视角。