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 mu M) 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 mu M 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.