铝诱导的烟草活性氧代谢及一氧化氮调控机制研究

Aluminum (Al) toxicity is a major factor limiting crop productivity on acid soils. Al-induced reactive oxygen species (ROS) metabolism has received great attention in the field of Al toxicity and resistance mechanisms. However, information about the mechanism of ROS generation and elimination caused by Al, and its regulation is scanty and unsystematic. In this item, two tobacoo cultivars differing in Al resistance were used to investigate the photosynthesis (including light energy allocation, noncyclic electron transport and carbon assimilation), respiration (including cytochrome respiration, activities of cytochrome oxidase and membrane complexes I and III), energy dissipation pathways and ROS metabolism in chloroplast and mitochondria, in order to elucidate the relationship between the mechanism of ROS generation/elimination from energy metabolism in chloroplast and mitochondria and Al toxicity/resistance in plants. And we paid great attention to energy dissipation pathways including heat dissipation from antenna in PSII, water-water cycle, photorespiration and cyclic flow of electron in chloroplast, and alternate respiration and alternative oxidase activity in mitochondria. At the same time, the regulatory mechanism of nitric oxide application on ROS generation/elimination in chloroplast and mitochondria was also examined. Through researches mentioned above, it may further enrich the mechanism of Al phytotoxicity and resistance, and provide theoretical and practical basis for enhancing Al resistance in plants with application of exogenous substances such as nitric oxide.

铝毒是酸性土壤上限制作物生长的主要因素。铝诱导的细胞活性氧代谢是该领域的研究热点之一，但对于铝是如何引起细胞内活性氧产生、清除及其调控机制的研究较少且无系统性。本项目拟以2个耐铝性差异显著的烟草品种为材料，从细胞器水平和能量代谢角度入手，研究铝胁迫下烟草光合作用（光能分配、非环式电子传递、碳同化）、呼吸作用（细胞色素呼吸、细胞色素氧化酶活性、膜复合体I和III活性）、叶绿体和线粒体内能量耗散途径（天线色素热耗散、水-水循环、光呼吸、环式电子传递；交替呼吸、交替氧化酶活性）、活性氧代谢等方面的变化，阐明烟草叶绿体和线粒体内能量代谢过程中活性氧的产生、清除机制与植物铝毒害/耐铝性的关系。同时研究一氧化氮对烟草叶绿体和线粒体内活性氧产生和清除的调控机制在增强植物耐铝性中的作用。通过上述研究，可望进一步丰富植物铝毒害及耐性机理，也可为利用一氧化氮等外源调控措施增强植物耐铝性提供理论依据和实践基础。

铝毒是限制酸性土壤上作物生长的最主要因素。其中，铝诱导的细胞活性氧代谢及其调控机制一直是植物铝毒害/耐铝性研究的热点。本项目以云烟100（耐铝）和云烟105（铝敏感）为材料，系统地研究了铝胁迫下烟草叶片叶绿体和线粒体内能量代谢和活性氧含量变化及其一氧化氮调控机制。研究结果表明：铝浓度的升高显著降低了烟草叶片净光合速率、最大光化学效率、PSII光合电子传递量子效率、光化学猝灭系数和细胞色素呼吸，提高了叶绿体和线粒体内过剩激发能，从而导致叶片活性氧含量升高，植株生物量下降，其中对云烟105影响大于云烟100。与此同时，烟草叶片非光化学猝灭系数、光呼吸、交替呼吸、超氧化物歧化酶和抗坏血酸过氧化物酶活性呈先升后降，有利于降低活性氧含量。外施一氧化氮（NO）可有效缓解铝对烟草的毒害，其作用机制为NO可通过提高烟草叶片光化学反应能力、热耗散、光呼吸、交替呼吸以及抗氧化酶活性来降低叶绿体和线粒体内过剩激发能，防止或清除烟草体内活性氧的产生和积累，且这种缓解效应在敏感基因型云烟105中表现更明显。本项目从细胞器水平和能量代谢角度出发阐明了铝引起细胞内活性氧产生、清除及其调控机制，进一步丰富了植物铝毒害/耐性机理，也为利用一氧化氮等化学调控措施增强植物耐铝性提供了理论和实践依据。