Oxidizes specifically succinate semialdehyde. Involved in plant response to environmental stress by preventing the accumulation of reactive oxygen species, probably by regulating proline, gamma-hydroxybutyrate (GHB) and gamma-aminobutyrate (GABA) levels (PubMed:15642352). Required for the maintenance of the shoot apical meristem (SAM) structure and subsequent adaxial-abaxial axis-dependent development of cotyledons and leaves (PubMed:21690177, PubMed:25840087). H2O + NAD(+) + succinate semialdehyde = 2 H(+) + NADH + succinate Competitive inhibition by NADH. Inhibited by ATP, ADP and AMP. Redox-regulated. Inhibited under oxydizing conditions (By similarity). Optimum pH is 9-9.5. Amino-acid degradation; 4-aminobutanoate degradation. Homotetramer. Expressed in developing leaf tissues. Induced during cold (4 degrees Celsius) acclimation (PubMed:17461790). Induced by salt (NaCl) (PubMed:20122158). Plants are sensitive to UVB and heat stress, and accumulate elevated levels of H(2)O(2) (PubMed:12740438). High light-dependent increased of proline, gamma-hydroxybutyrate (GHB) and gamma-aminobutyrate (GABA) levels. Treatment with gamma-vinyl-gamma-aminobutyrate, a specific gamma-aminobutyrate (GABA)-transaminase inhibitor, prevents the accumulation of reactive oxygen intermediates (ROI) and GHB in ssadh mutants, inhibits cell death, and improves growth (PubMed:15642352). The ssadh mutant defects associated with stress responses are suppressed by POP2 disruption (PubMed:18846220). In enf1, pleiotropic developmental defects including dwarfism, and abnormal leaf shape (including abaxialized and adaxialized leaves) and cotyledon associated with altered GABA and SucA levels in shoots; these phenotypes are partially suppressed by the disruption of POP2/GABAT1, GSA1, GSA2 and HEMA1 (PubMed:21690177, PubMed:25840087). Abnormal FIL expression, especially in the adaxial side, in the leaf primordia (PubMed:21690177). Belongs to the aldehyde dehydrogenase family.