The element arsenic (As) is a non-essential metalloid that is found naturally in all soils and at high concentrations it is toxic to plant cells. As (V) can act as a chemical analogue of phosphate, it can disrupt phosphate-related energy metabolism and lipid structure. In this study, the contribution of mitochondrial alternative oxidase (AOX) and chloroplastic plastid terminal oxidase (PTOX) to As (V) stress tolerance was investigated. Our data indicate that As (V) stress (100, 200 and 300 µM) induces AOX gene expression by 3.3- to 10.5-fold depending on AOX gene, but not PTOX expression in wild-type A. thaliana plants. To further elucidate the role of AOX in As (V) stress tolerance, we utilized aox1a mutants and observed that aox1a mutants had decreased growth and higher oxidative stress damage under stress conditions, while there were no differences under control conditions. Moreover, acclimation of aox1a plants to new cellular redox environment was investigated by measuring the activities of reactive oxygen species (ROS)-scavenging enzymes. Induction of mitochondrial MnSOD activity at 300 µM As (V) was higher in aox1a plants (70%), when compared to wild type (43%). However, total ascorbate peroxidase and dehydroascorbate reductase activities were lower in aox1a plants when compared to wild type, which might explain higher oxidative damage observed in this genotype. On the other hand, NADPH oxidase activity, which is involved in ROS signaling, was lower in aox1a plants under normal conditions but a higher induction was observed with As (V) stress. Overall, our data indicate that AOX1a is involved in adaptation to As (V)-induced oxidative stress.

中文翻译：

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线粒体替代氧化酶（AOX1a）是缓解拟南芥中砷诱导的氧化应激所必需的

砷（As）是一种非必需的准金属，在所有土壤中都自然存在，并且高浓度对植物细胞有毒。由于（V）可以充当磷酸盐的化学类似物，因此它可以破坏磷酸盐相关的能量代谢和脂质结构。在这项研究中，线粒体替代氧化酶（AOX）和叶绿体质体末端氧化酶（PTOX）对As（V）胁迫耐受性的贡献进行了研究。我们的数据表明，随着（V）应力（100，200和300μM）诱导AOX取决于由3.3-基因表达10.5倍AOX基因，但不PTOX在野生型表达拟南芥植物。为了进一步阐明AOX在As（V）胁迫耐受性中的作用，我们利用了aox1a突变体，并观察到aox1a突变体在胁迫条件下生长减少，氧化应激损伤更高，而对照条件下没有差异。此外，通过测量活性氧清除酶的活性，研究了aox1a植物适应新的细胞氧化还原环境的能力。与野生型（43％）相比，aox1a植物（70％）在300 µM As（V）下的线粒体MnSOD活性更高。但是，aox1a中的总抗坏血酸过氧化物酶和脱氢抗坏血酸还原酶活性较低与野生型植物相比，可能解释了该基因型中较高的氧化损伤。另一方面，在正常条件下，aox1a植物中参与ROS信号传导的NADPH氧化酶活性较低，但在As（V）胁迫下观察到较高的诱导。总体而言，我们的数据表明AOX1a参与了对砷（V）诱导的氧化应激的适应。