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To understand the tolerance to salinity and osmoregulation of the introduced Trachemys scripta elegans, the salinity stress of four groups (salinity 5‰, 15‰, 25‰and control group) were conducted. Inorganic ions, osmotic pressure, glucose and aldosterone of blood and urine in T. s. elegans (BW:125.60 ± 19.84 g) were analyzed at 30 d, 60 d and 90 d stress. The results showed that:1) inorganic ions concentration of blood and urine increased with ambient salinity, which indicated that high inlfux of ions was combined with higher outlfow when exposed to saline water in T. s. elegans. However, blood aldosterone decreased with increasing salinity, which indicated that an increased sodium intake resulting in a diminished aldosterone production. However, with elapsed time, inorganic ions in urine decreased, which indicated that inorganic ions in blood would be accumulated, and Na+and Cl-in the plasma inevitably build up to harmful levels, at last death was happening when T. s. elegans was exposed to salinity 25 during 90 d salinity stress;2) blood osmotic pressure increased as ambient salinity increased, it would reach 400 mOsm/kg in the group of salinity 25, which was about 1.5 fold of the control group. Higher blood osmotic pressure was due to both higher blood ions and urea concentrations. There may be another mechanism to avoid an excess of NaCl together with an important loss of water using one of the end-products of nitrogen metabolism;3) blood glucose in each group except the group of salinity 5 decreased with time elapsed and with salinity increased. Therefore, we can conclude that T. s. elegans is an osmoregulator that limits the entry of Na+and Cl-, but can also tolerate certain degrees of increases in plasma Na+and Cl-. When ambient salinity was lower than 15‰, T. s. elegans can increase blood osmotic pressure by balancing the entry of NaCl with the secretion of aldosterone decreased, and by accumulating blood urea for osmoregulation effectors, and survive for at least three months. These results could provide theoretical basis for salinity tolerance and the invasion on physiological mechanism for T. s. elegans.