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大肠杆菌硝酸盐还原培养物中依赖亚铁的一氧化氮生成

Ferrous iron dependent nitric oxide production in nitrate reducing cultures of Escherichia coli.

作者信息

Brons H J, Hagen W R, Zehnder A J

机构信息

Department of Microbiology, Wageningen Agricultural University, The Netherlands.

出版信息

Arch Microbiol. 1991;155(4):341-7. doi: 10.1007/BF00243453.

Abstract

L-Lactate-driven ferric and nitrate reduction was studied in Escherichia coli E4. Ferric iron reduction activity in E. coli E4 was found to be constitutive. Contrary to nitrate, ferric iron could not be used as electron acceptor for growth. "Ferric iron reductase" activity of 9 nmol Fe2+ mg-1 protein min-1 could not be inhibited by inhibitors for the respiratory chain, like Rotenone. Quinacrine, Actinomycin A, or potassium cyanide. Active cells and L-lactate were required for ferric iron reduction. The L-lactate-driven nitrate respiration in E. coli E4 leading to the production of nitrite, was reduced to about 20% of its maximum activity with 5 mM ferric iron, or to about 50% in presence of 5 mM ferrous iron. The inhibition was caused by nitric oxide formed by a purely chemical reduction of nitrite by ferrous iron. Nitric oxide was further chemically reduced by ferrous iron to nitrous oxide. With electron paramagnetic resonance spectroscopy, the presence of a free [Fe2(+)-NO] complex was shown. In presence of ferrous or ferric iron and L-lactate, nitrate was anaerobically converted to nitric oxide and nitrous oxide by the combined action of E. coli E4 and chemical reduction reactions (chemodenitrification).

摘要

在大肠杆菌E4中研究了L-乳酸驱动的铁离子和硝酸根还原过程。发现大肠杆菌E4中的铁离子还原活性是组成型的。与硝酸根不同,铁离子不能用作生长的电子受体。9 nmol Fe2+ mg-1蛋白质·分钟-1的“铁离子还原酶”活性不能被呼吸链抑制剂如鱼藤酮、奎纳克林、放线菌素A或氰化钾抑制。铁离子还原需要活细胞和L-乳酸。大肠杆菌E4中L-乳酸驱动的硝酸根呼吸作用导致亚硝酸盐的产生,在5 mM铁离子存在下,其最大活性降低至约20%,在5 mM亚铁离子存在下降低至约50%。这种抑制是由亚铁离子将亚硝酸盐完全化学还原形成的一氧化氮引起的。一氧化氮进一步被亚铁离子化学还原为一氧化二氮。通过电子顺磁共振光谱法,显示了游离[Fe2(+)-NO]配合物的存在。在亚铁离子或铁离子和L-乳酸存在下,通过大肠杆菌E4的联合作用和化学还原反应(化学反硝化作用),硝酸根被厌氧转化为一氧化氮和一氧化二氮。

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