Soil salinity is the primary factor restricting plant growth and development. In this study, the morpho-physiological, biochemical, and molecular responses of turnip seedlings to three distinct salt stress treatments were investigated: no salinity 0 mM, moderate salinity at 80 mM, and severe salinity at 160 mM. Gibberellic acid treatments were applied in three different concentrations: control, 1 mM, and 2 mM. The dry and fresh weights, shoot and root lengths, carotenoid and chlorophyll levels, K+ ion accumulation, and antioxidant enzyme activity were all decreased by salt stress, particularly at 200 mM. However, it accelerated the buildup of Na+ ions and oxidative damage. Application of gibberellic acid enhanced turnip development under salt stress. Compared with the control, the gibberellic acid-2mM recorded the highest increase in roots and shoots length (16.79-10.80%), shoots fresh and dry weights (15.21-28.39%), chlorophyll a and b (7.49-15.94%), SOD and POD (16.92-10.85%), yield weight and diameter (18.33-10.11%) during different salinity levels. This treatment also reduced the MDA and H2O2 content (15.12-10.58%), and Na+ ions in roots and leaves (20.20-5.44%). Based on these findings, gibberellic acid at a concentration of 2 mM may be a useful tool for enhancing turnip development and growth.

Gibberellic acid (GA3), one of the most plant growth stimulator, is widely applied in agricultural regions and in beer industry. However, GA3 residue remained in soil and water can cause toxicity to all organisms. In this study, we investigated the mechanisms of GA3-induced hepatic injury in gibel carp (Carassius auratus gibelio). We found that GA3 exposure caused oxidative stress, endoplasmic reticulum stress (ERS), and apoptosis. The gibel carp exposed to GA3 exhibited significant alteration in erythrocyte nuclei. GA3 induced liver damage, as indicated by increasing the aminopherase activities. GA3 led to oxidative stress by increasing malondialdehyde content and decreasing the activities of CAT and GPx. GA3 stimulated ERS and increased the expression of grp78, perk, eif2s1 alpha, chop, atf4, ire1 alpha, xbp1, and atf6. Additionally, GA3 down-regulated the level of anti-apoptotic gene Bcl2 and up-regulated the levels of pro-apoptotic genes bax and caspase-3. Overall results demonstrated that GA3 caused hepatic injury in gibel carp by increasing oxidative stress, ERS, and apoptosis.