钙离子对盐胁迫小麦幼苗氮代谢的影响

为探讨增强小麦抗盐能力的调控途径,以普通小麦豫麦34为材料,研究了Ca2+对盐胁迫下小麦幼苗氮代谢及生长的影响.采用全营养液培养小麦幼苗至第一片叶完全展开,更换无钙营养液,并开始不同处理.处理分别为低盐胁迫(150 mmol · L-1 NaCl)、低盐胁迫+4 mmol · L-1 Ca2+、高盐胁迫(300 mmol · L-1 NaCl)、高盐胁迫+4mmol · L-1 Ca2+,以无NaCl胁迫的小麦为对照.5 d后取样,测定了氮同化酶活性、代谢物含量、积累量及幼苗生长状况.结果表明,Ca2+明显缓解了低盐胁迫对小麦幼苗的生长抑制,表现在鲜重、叶绿素及可溶性蛋白含量的增加,而对高盐胁迫下小麦幼苗的生长无明显改善效果;Ca2+改善了低盐胁迫下小麦幼苗的氮营养状况,表现在氮积累量的增加,这一效应主要是通过硝酸还原酶(NR)、谷氨酰胺合成酶(GS)以及异柠檬酸脱氢酶(NADP-ICDH)活性的增强而实现的.Ca2+未能改善高盐胁迫下小麦幼苗氮营养状况的主要限制因子在于NADP-ICDH活性未明显增加.

Effects of Ca2+ on nitrogen metabolism in wheat seedlings exposed to salt stress

To seek ways for improving salt\|tolerance of wheat plants, experiments were conducted to examine the ameliorative effects of Ca2+ on nitrogen metabolism under salt stress using an ordinary wheat cultivar (Triticum aestivum L. cv. Yumai 34) as the material. The wheat seedlings were cultured in full nutrient solution. The first leaf being fully expanded, different treatments were initiated by culturing the plants in the nutrient solution without calcium. NaCl (150 mmol?L-1 and 300 mmol?L-1) and combinations of NaCl + Ca2+ (150 mmol?L-1 + 4 mmol?L-1 and 300 mmol?L-1 + 4 mmol?L-1) were applied to the growing plants using no salt\|stressed plants as control. After 5 days of treatments, the activities of nitrogen assimilation enzymes, the amount of nitrogen assimilation and the growth status of wheat seedlings were determined. The results showed that Ca2+ significantly alleviated the depressed\|growth of wheat seedlings under low salt stress, manifesting the enhanced fresh weight, chlorophyll and soluble protein contents; while Ca2+ did not show obvious ameliorative effects under high salt stress. Ca2+ promoted the nitrogen assimilation and improved the status of nitrogen nutrition in wheat plants exposed to low salt stress, which could be mainly due to the enhanced activities of nitrate reductase (NR), glutamine synthetase (GS) and NADP\|dependent isocitrate dehydrogenase (NADP\|ICDH). The minor ameliorative effects of Ca2+ on nitrogen assimilation in wheat seedlings under high salt stress could be explained by the insignificant increase of NADP\|ICDH activity.