Changes in the antioxidant systems as part of the signaling pathway responsible for the programmed cell death activated by nitric oxide and reactive oxygen species in tobacco Bright-Yellow 2 cells.
Nitric oxide (NO) has been postulated to be required, together with reactive oxygen species (ROS), for the activation of the hypersensitive reaction, a defense response induced in the noncompatible plant-pathogen interaction. However, its involvement in activating programmed cell death (PCD) in plant cells has been questioned. In this paper, the involvement of the cellular antioxidant metabolism in the signal transduction triggered by these bioactive molecules has been investigated. NO and ROS levels were singularly or simultaneously increased in tobacco (Nicotiana tabacum cv Bright-Yellow 2) cells by the addition to the culture medium of NO and/or ROS generators. The individual increase in NO or ROS had different effects on the studied parameters than the simultaneous increase in the two reactive species. NO generation did not cause an increase in phenylalanine ammonia-lyase (PAL) activity or induction of cellular death. It only induced minor changes in ascorbate (ASC) and glutathione (GSH) metabolisms. An increase in ROS induced oxidative stress in the cells, causing an oxidation of the ASC and GSH redox pairs; however, it had no effect on PAL activity and did not induce cell death when it was generated at low concentrations. In contrast, the simultaneous increase of NO and ROS activated a process of death with the typical cytological and biochemical features of hypersensitive PCD and a remarkable rise in PAL activity. Under the simultaneous generation of NO and ROS, the cellular antioxidant capabilities were also suppressed. The involvement of ASC and GSH as part of the transduction pathway leading to PCD is discussed.
de Pinto
Maria Concetta
MC
Dipartimento di Biologia e Patologia Vegetale, Via E. Orabona 4, I-70125 Bari, Italy.
Tommasi
Franca
F
De Gara
Laura
L
D000975:Antioxidants / Q000378:metabolism*; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology*; D060387:Ascorbate Peroxidases; D001205:Ascorbic Acid / Q000378:metabolism; D002460:Cell Line; D002478:Cells, Cultured; D005947:Glucose / Q000494:pharmacology; D005949:Glucose Oxidase / Q000494:pharmacology; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D007113:Immunity, Innate / Q000187:drug effects; D015227:Lipid Peroxidation / Q000187:drug effects; D009247:NADH, NADPH Oxidoreductases / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D009599:Nitroprusside / Q000494:pharmacology; D010084:Oxidation-Reduction / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects; D010088:Oxidoreductases / Q000378:metabolism; D010544:Peroxidases / Q000378:metabolism; D010650:Phenylalanine Ammonia-Lyase / Q000378:metabolism; D010935:Plant Diseases / Q000382:microbiology; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*; D014026:Nicotiana / Q000166:cytology / Q000378:metabolism*
D000975:Antioxidants; D017382:Reactive Oxygen Species; D009599:Nitroprusside; D009569:Nitric Oxide; D006861:Hydrogen Peroxide; D010088:Oxidoreductases; D005949:Glucose Oxidase; D010544:Peroxidases; D060387:Ascorbate Peroxidases; D009247:NADH, NADPH Oxidoreductases; C023927:monodehydroascorbate reductase (NADH); D005980:Glutathione Reductase; C020666:glutathione dehydrogenase (ascorbate); D010650:Phenylalanine Ammonia-Lyase; D005978:Glutathione; D005947:Glucose; D001205:Ascorbic Acid; D019803:Glutathione Disulfide