Abscisic acid-induced thermotolerance in maize seedlings is mediated by calcium and associated with antioxidant systems

ABA treatment significantly increased thermotolerance in maize seedlings. Pretreatment of maize seeds with CaCl2 solution, which raises calcium content of maize seedlings, further enhanced the ABA-induced thermotolerance. In contrast, pretreatment with the Ca2+ chelator EGTA, which lowers calcium content of maize seedlings, decreased the ABA-induced thermotolerance. In addition, pretreatment with the plasma membrane Ca2+ channel blockers La3+ and verapamil, which are expected to inhibit the influx of extracellular Ca2+ into cells, also weakened the ABA-induced thermotolerance in maize seedlings. However, the calmodulin antagonists W7 and CPZ had little effect on the ABA-induced thermotolerance. Measurement of activities of the antioxidant enzymes SOD, CAT, APX and GPX and the level of lipid peroxidation (in terms of MDA) indicated that heat stress induced an oxidative stress in maize seedlings. ABA treatment enabled maize seedlings to maintain higher activities of these antioxidant enzymes and a lower level of lipid peroxidation at normal culture temperature and under heat stress. Ca2+ pretreatment further enhanced the ABA-induced increase in SOD and APX activities and lowered the heat stress-induced lipid peroxidation in the ABA-treated seedlings, but EGTA pretreatment had a contrary effect. These results suggest that the ABA-induced thermotolerance is mediated by Ca2+ and requires the entry of extracellular Ca2+ into cells across the plasma membrane; antioxidant enzyme systems take part in the final generation of the ABA-induced thermotolerance.