Background and Aims: Eutrema parvulum (synonym, Thellungiella parvula) is an extreme halophyte that thrives in high salt concentrations (100-150 mM) and is closely related to Arabidopsis thaliana. The main aim of this study was to determine how E. parvulum uses reactive oxygen species (ROS) production, antioxidant systems and redox regulation of the electron transport system in chloroplasts to tolerate salinity. Methods: Plants of E. parvulum were grown for 30 d and then treated with either 50, 200 or 300 mM NaCl. Physiological parameters including growth and water relationships were measured. Activities of antioxidant enzymes were determined in whole leaves and chloroplasts. In addition, expressions of chloroplastic redox components such as ferrodoxin thioredoxin reductases (FTR), NADPH thioredoxin reductases (NTRC), thioredoxins (TRXs) and peroxiredoxins (PRXs), aswell as genes encoding enzymes of thewater-water cycle and proline biosynthesis were measured. KeyResults: Salt treatment affectedwater relationships negativelyand the accumulation of prolinewas increased by salinity. E. parvulum was able to tolerate 300 mM NaCl over long periods, as evidenced by H2O2 content and lipid peroxidation. While Ca2+ and K+ concentrationswere decreased by salinity, Na+ and Cl-concentrations increased. Efficient induction of activities and expressions ofwater-water cycle enzymes might prevent accumulation of excess ROS in chloroplasts and therefore protect the photosynthetic machinery in E. parvulum. The redox homeostasis in chloroplasts might be achieved by efficient induction of expressions of redox regulatory enzymes such as FTR, NTRC, TRXs and PRXs under salinity. Conclusions: E. parvulumwas able to adapt to osmotic stress by an efficient osmotic adjustment mechanism involving proline and was able to regulate its ion homeostasis. In addition, efficient induction ofwater-water cycle enzymes and other redox regulatory components such as TRXs and PRXs in chloroplasts were able to protect the chloroplasts from salinity-induced oxidative stress.