摘要
以‘吉塞拉5号’樱桃组培苗为试材,研究短期低氧胁迫下氮对樱桃幼苗根系抗氧化酶活性及线粒体功能的影响。通过溶氧调节仪人为控制营养液溶氧浓度为2mg·L-1,NO3-浓度共设4个水平:0、7.5、15.0、22.5mmol·L-1,以1/2 Hoagland营养液正常低氧处理(NO3-浓度7.5mmol·L-1)为对照。结果表明:各处理SOD、POD、CAT酶活性均呈现先升高后降低的趋势。与对照相比,营养液加氮处理的SOD、POD、CAT酶活性升高,膜质过氧化程度减轻,且氮浓度越大酶活性升高幅度越大,而营养液缺氮处理的酶活性降低,膜质过氧化程度加重;营养液缺氮处理樱桃根系线粒体中的H2O2和MDA含量、O2·-生成速率升高,而营养液加氮处理可降低O2.-的产生及MDA含量,提高线粒体的氧化磷酸化水平,保护樱桃根系线粒体膜的完整性,对线粒体呼吸功能的破坏明显减轻,且NO3-离子浓度高时效果更好,说明适当提高营养液中的氮素水平可以缓解低氧胁迫对樱桃根系的伤害。
The purpose of this paper is to explore the effects of exogenous application nitrogen in nutrient solution on the activity of antioxidant enzymes and function of mitochondria in cherry rootstock roots under hypoxia stress. The cherry rootstock seedlings were cultured in 1/2 Hogland nutrient solutions of different NO3^-concentration (0,7.5,15.0,22.5 mmol·L^-1. The oxygen concentration of the nutrient solution dissolved was controlled 2 mg·L-1. Under the normal oxygen condition,7.5 mmol·L^-1NO3^-was a control. The results showed that the activities of SOD,POD and CAT of cherry rootstock roots in the four treatments were all increased at the first four days and then decreased. Compared with the control,the activities of SOD,POD and CAT of cherry rootstock roots after the treatment with 15 or 22.5 mmol·L^-1NO3^-increased and the MDA content decreased. The contents of H2O2 and MDA,production rate of O2·^-in mitochondria of the treatment with nitrogen deficiency were the most among the four treatments. Additional nitrogen into the nutrient solution under hypoxia stress could decrease contents of H2O2 and MDA,production rate of O2·^-and increase the cytochrome c/a and the rate of respiration of mitochondria by increasing respiratory control ratio and oxidative phosphorilation ratio. The above results suggested that exogenous nitrogen application in nutrient solution could antagonize the damage of hypoxia stress on cherry seedlings.
出处
《园艺学报》
CAS
CSCD
北大核心
2009年第11期1575-1580,共6页
Acta Horticulturae Sinica
基金
江苏省自然科学基金项目(BK2009717)
关键词
樱桃
低氧胁迫
氮
抗氧化酶
线粒体
cherry
hypoxia stress
nitrogen
antioxidant enzymes
mitochondria