Chloroplastic oxidative burst induced by tenuazonic acid, a natural photosynthesis inhibitor, triggers cell necrosis in Eupatorium adenophorum Spreng
| Autor: | Fenyan Zhou, Chunyan Yin, Shiguo Chen, Sheng Qiang, Xinbin Dai |
|---|---|
| Rok vydání: | 2010 |
| Předmět: |
Chloroplasts
TeA Biophysics Tenuazonic Acid DNA Fragmentation Biology Photosynthesis Thylakoids Chloroplast Biochemistry Lipid peroxidation Necrosis chemistry.chemical_compound Phytotoxin Superoxides Tenuazonic acid Ageratina Cellular compartment Respiratory Burst chemistry.chemical_classification Reactive oxygen species Antibiotics Antineoplastic Photosynthesis inhibitor Hydroxyl Radical Electron Spin Resonance Spectroscopy Photosystem II Protein Complex food and beverages ROS Hydrogen Peroxide Cell Biology Electron transport chain Chromatin Plant Leaves Oxidative Stress chemistry Mode of action Thylakoid Lipid Peroxidation Reactive Oxygen Species Oxidation-Reduction |
| Zdroj: | Biochimica et Biophysica Acta (BBA) - Bioenergetics. 1797:391-405 |
| ISSN: | 0005-2728 |
| DOI: | 10.1016/j.bbabio.2009.12.007 |
| Popis: | Tenuazonic acid (TeA), a nonhost-specific phytotoxin produced by Alternaria alternata, was determined to be a novel natural photosynthesis inhibitor owning several action sites in chloroplasts. To further elucidate the mode of its action, studies were conducted to assess the production and involvement of reactive oxygen species (ROS) in the toxic activity of TeA. A series of experiments indicated that TeA treatment can induce chloroplast-derived ROS generation including not only (1)O(2) but also superoxide radical, H(2)O(2) and hydroxyl radicals in Eupatorium adenophorum mesophyll cells, resulting from electron leakage and charge recombination in PSII as well as thylakoid overenergization due to inhibition of the PSII electron transport beyond Q(A) and the reduction of end acceptors on the PSI acceptor side and chloroplast ATPase activity. The initial production of TeA-induced ROS was restricted to chloroplasts and accompanied with a certain degree of chloroplast damage. Subsequently, abundant ROS were quickly dispersed throughout whole cell and cellular compartments, causing a series of irreversible cellular harm such as chlorophyll breakdown, lipid peroxidation, plasma membrane rupture, chromatin condensation, DNA cleavage, and organelle disintegration, and finally resulting in rapid cell destruction and leaf necrosis. These results show that TeA causing cell necrosis of host-plants is a result of direct oxidative damage from chloroplast-mediated ROS eruption. |
| Databáze: | OpenAIRE |
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