The two As resistance arsRBC operons of Pseudomonas putida KT2440 are followed by a downstream gene called arsH that encodes an NADPH‐dependent flavin mononucleotide reductase. In this work, we show that the arsH1 and (to a lesser extent) arsH2 genes of P. putida KT2440 strengthened its tolerance to both inorganic As(V) and As(III) and relieved the oxidative stress undergone by cells exposed to either oxyanion. Furthermore, overexpression of arsH1 and arsH2 endowed P. putida with a high tolerance to the oxidative stress caused by diamide (a drainer of metabolic NADPH) in the absence of any arsenic. To examine whether the activity of ArsH was linked to a direct action on the arsenic compounds tested, arsH1 and arsH2 genes were expressed in Escherichia coli , which has an endogenous arsRBC operon but lacks an arsH ortholog. The resulting clones both deployed a lower production of reactive oxygen species (ROS) when exposed to As salts and had a superior endurance to physiological redox insults. These results suggest that besides the claimed direct action on organoarsenicals, ArsH contributes to relieve toxicity of As species by mediating reduction of ROS produced in vivo upon exposure to the oxyanion, e.g. by generating FMNH₂ to fuel ROS‐quenching activities.

中文翻译：

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ArsH保护恶臭假单胞菌免受因接触砷引起的氧化损伤。

恶臭假单胞菌KT2440的两个As抗性arsRBC操纵子后接一个称为arsH的下游基因，该基因编码NADPH依赖性黄素单核苷酸还原酶。在这项工作中，我们表明恶臭假单胞菌KT2440的arsH1和arsH2基因（在较小程度上）增强了其对无机As（V）和As（III）的耐受性，并减轻了暴露于任何一种氧阴离子的细胞遭受的氧化应激。此外，arsH1和arsH2的过表达赋予恶臭假单胞菌在没有任何砷的情况下，对由二酰胺（代谢NADPH的排出物）引起的氧化应激具有很高的耐受性。为了检查ArsH的活性是否与对所测试的砷化合物的直接作用有关，在具有内源性arsRBC操纵子但缺乏arsH直系同源物的大肠杆菌中表达了arsH1和arsH2基因。当暴露于As盐时，所得克隆都具有较低的活性氧（ROS）产生量，并且对生理氧化还原损伤具有较高的耐受性。这些结果表明，除了要求的对有机砷的直接作用外，ArsH还通过介导产生的ROS的减少来缓解As物种的毒性。在体内暴露于氧阴离子后，例如通过生成FMNH ₂来促进ROS猝灭活性。