Ruiz-Herrera J, DeMoss J A
J Bacteriol. 1969 Sep;99(3):720-9. doi: 10.1128/jb.99.3.720-729.1969.
The participation of distinct formate dehydrogenases and cytochrome components in nitrate reduction by Escherichia coli was studied. The formate dehydrogenase activity present in extracts prepared from nitrate-induced cells of strain HfrH was active with various electron acceptors, including methylene blue, phenazine methosulfate, and benzyl viologen. Certain mutants which are unable to reduce nitrate had low or undetectable levels of formate dehydrogenase activity assayed with methylene blue or phenazine methosulfate as electron acceptor. Of nine such mutants, five produced gas when grown anaerobically without nitrate and possessed a benzyl viologen-linked formate dehydrogenase activity, suggesting that distinct formate dehydrogenases participate in the nitrate reductase and formic hydrogenlyase systems. The other four mutants formed little gas when grown anaerobically in the absence of nitrate and lacked the benzyl viologen-linked formate dehydrogenase as well as the methylene blue or phenazine methosulfate-linked activity. The cytochrome b(1) present in nitrate-induced cells was distinguished by its spectral properties and its genetic control from the major cytochrome b(1) components of aerobic cells and of cells grown anaerobically in the absence of nitrate. The nitrate-specific cytochrome b(1) was completely and rapidly reduced by 1 mm formate but was not reduced by 1 mm reduced nicotinamide adenine dinucleotide; ascorbate reduced only part of the cytochrome b(1) which was reduced by formate. When nitrate was added, the formate-reduced cytochrome b(1) was oxidized with biphasic kinetics, but the ascorbate-reduced cytochrome b(1) was oxidized with monophasic kinetics. The inhibitory effects of n-heptyl hydroxyquinoline-N-oxide on the oxidation of cytochrome b(1) by nitrate provided evidence that the nitrate-specific cytochrome is composed of two components which have different redox potentials but identical spectral properties. We conclude from these studies that nitrate reduction in E. coli is mediated by the sequential operation of a specific formate dehydrogenase, two specific cytochrome b(1) components, and nitrate reductase.
研究了不同的甲酸脱氢酶和细胞色素成分在大肠杆菌硝酸盐还原过程中的参与情况。从菌株HfrH的硝酸盐诱导细胞制备的提取物中存在的甲酸脱氢酶活性,对包括亚甲蓝、吩嗪硫酸甲酯和苄基紫精在内的各种电子受体具有活性。某些无法还原硝酸盐的突变体,以亚甲蓝或吩嗪硫酸甲酯作为电子受体测定时,甲酸脱氢酶活性水平较低或无法检测到。在九个这样的突变体中,有五个在无氧且无硝酸盐的条件下生长时会产生气体,并具有与苄基紫精相连的甲酸脱氢酶活性,这表明不同的甲酸脱氢酶参与了硝酸盐还原酶和甲酸氢解酶系统。另外四个突变体在无氧且无硝酸盐的条件下生长时几乎不产生气体,并且缺乏与苄基紫精相连的甲酸脱氢酶以及与亚甲蓝或吩嗪硫酸甲酯相连的活性。硝酸盐诱导细胞中存在的细胞色素b(1),通过其光谱特性及其遗传控制,与需氧细胞以及在无氧且无硝酸盐条件下生长的细胞中的主要细胞色素b(1)成分区分开来。硝酸盐特异性细胞色素b(1)能被1 mM甲酸完全且快速地还原,但不能被1 mM还原型烟酰胺腺嘌呤二核苷酸还原;抗坏血酸只能还原部分被甲酸还原的细胞色素b(1)。添加硝酸盐后,被甲酸还原的细胞色素b(1)以双相动力学被氧化,但被抗坏血酸还原的细胞色素b(1)以单相动力学被氧化。正庚基羟基喹啉-N-氧化物对硝酸盐氧化细胞色素b(1)的抑制作用提供了证据,表明硝酸盐特异性细胞色素由两个具有不同氧化还原电位但光谱特性相同的成分组成。我们从这些研究中得出结论,大肠杆菌中的硝酸盐还原是由一种特定的甲酸脱氢酶、两种特定的细胞色素b(1)成分和硝酸盐还原酶的顺序作用介导的。