###### Abstract  
Soybean (_Glycine max_) is an economically important crop which is very susceptible to salt stress. Tolerance to Na2 SO4 stress was evaluated in soybean plants overexpressing or suppressing the phytoglobin _GmPgb1_. Salt stress depressed several gas exchange parameters, including the photosynthetic rate, caused leaf damage, and reduced the water content and dry weights. Lower expression of respiratory burst oxidase homologs (_RBOHB_ and _D_), as well as enhanced antioxidant activity, resulting from _GmPgb1_ overexpression, limited ROS-induced damage in salt-stressed leaf tissue. The leaves also exhibited higher activities of the H2O2-quenching enzymes, catalase (CAT) and ascorbate peroxidase (APX), as well as enhanced levels of ascorbic acid. Relative to WT and _GmPgb1_-suppressing plants, overexpression of _GmPgb1_ attenuated the accumulation of foliar Na+ and exhibited a lower Na+/K+ ratio. These changes were attributed to the induction of the Na+ efflux transporter SALT OVERLY SENSITIVE 1 (SOS1) limiting Na+ intake and transport and the inward rectifying K+ channel POTASSIUM TRANSPORTER 1 (AKT1) required for the maintenance of the Na+/K+ balance. Keywords:antioxidant response; phytoglobin; reactive oxygen species; sodium sulfate; soybean; salinity tolerance; Na+/K+ balance : 11.10.70.  
nutrient deficiency, as well as damage of cellular components [7]. Oxidative stress is caused by excessive accumulation of reactive oxygen species (ROS) causing cellular damage [8]. The combination of these effects leads to two temporally separated responses. The initial inhibition of growth, occurring within hours as a result of depressed cell elongation and decreased stomatal conductance, is followed by damage resulting from nutritional imbalance and oxidative stress [9; 10]. Therefore, mitigation of nutritional imbalance through maintenance of ion homeostasis and attenuation of oxidative stress through the activation of antioxidant responses are desirable traits in salinity tolerance [11], also reported in soybean [5]. The main factor contributing to salinity stress is Na\({}^{+}\), which alters water management, damages cellular organelles and membranes, and impedes energetic and photosynthetic processes [12]. Besides depressing the activity of many enzymes involved in the synthesis of chlorophyll, Na\({}^{+}\) impairs components of the photosynthetic electron transport chain [13; 14] and proteins required for the reduction of CO\({}_{2}\)[15]. Many of these effects have been linked to the Na\({}^{+}\) disturbance in the cellular level of K\({}^{+}\) which is required in many photosynthetic functions [16]. Noxious levels of Na\({}^{+}\), in fact, not only competitively inhibit the K\({}^{+}\) influx, but also induce the K\({}^{+}\) efflux through depolarization of plasma membranes [17]. Therefore, maintenance of a low Na\({}^{+}\)/K\({}^{+}\) ratio through the retention of cellular K\({}^{+}\) and/or exclusion of Na\({}^{+}\) from sensitive tissues is a desirable trait of salt tolerance [18]. This notion is best exemplified by the acquired tolerance to salinity resulting from supplementation of K\({}^{+}\) or exclusion of cellular Na\({}^{+}\) through the upregulation of Na\({}^{+}\) efflux transporters [19; 20; 21; 22]. Besides altering the K\({}^{+}\) homeostasis, excess Na\({}^{+}\) causes oxidative stress through accumulation of reactive oxygen species (ROS) [8]. A soybean Na\({}^{+}\)/H\({}^{+}\) antiporter, SALT-OVERLY SENSITIVE 1 (SOS1), alleviated toxicity by limiting the Na\({}^{+}\) accumulation in leaves [22]. Overexpression of _SOS1_ also mitigated oxidative stress resulting from ROS accumulation [22]. Required at low levels to regulate many aspects of growth and development, ROS can become noxious if they exceed physiological thresholds, as observed during different conditions of stress, including salinity [23]. Elevated levels of ROS alter the function of membranes by oxidizing fatty acids and lipids and cause inhibition of enzymes and damage to nucleic acids.