| Abstrakt: |
Pretreatment of maize (Zea mays L.) seeds with CaCl2 solution significantly raised calcium and calmodulin levels and enhanced intrinsic heat tolerance in maize seedlings. This enhancement is specific to Ca2+ and cannot be substituted by Mg2+. In contrast, treatments with the Ca2+ chelator EGTA or plasma membrane Ca2+ channel blockers La3+ or verapamil lowered the intrinsic heat tolerance. Concurrent treatment with Ca2+ and Ca2+ -channel blockers (La3+, verapamil) also decreased the Ca2+ -enhanced heat tolerance. In addition, calmodulin antagonists chlorpromazine or W7 treatment eliminated the Ca2+ -enhanced heat tolerance, whilst W5, a less active analogue of W7, had little effect on the Ca2+ -enhanced heat tolerance. Measurement of antioxidant enzyme activities and lipid peroxidation showed that heat stress induced an oxidative stress in maize seedlings. External Ca2+ treatment enabled the seedlings to keep relatively higher activities of superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX) and lower levels of lipid peroxidation than Ca2+ -deficient treatments; on the contrary, EGTA treatment led to more rapid loss of SOD, CAT and APX activities and higher levels of lipid peroxidation in the seedlings under heat stress. In addition, concurrent Ca2+ and W7 treatment weakened the effects of Ca2+ treatment on SOD, CAT and APX activities and caused more severe lipid peroxidation. These results suggested that external Ca2+ can enhance the intrinsic heat tolerance of maize seedlings. This enhancement requires the entry of external Ca2+ into cells across plasma membranes and the mediation of intracellular calmodulin, and is associated with the increase of antioxidant system activity. |
