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

Abstract

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.

Proline and Glycinebetaine Ameliorated NaCl Stress via Scavenging of Hydrogen Peroxide and Methylglyoxal but Not Superoxide or Nitric Oxide in Tobacco Cultured Cells

“…16) On the other hand, NaCl has been found to decrease the NO level by inhibiting NO synthase activity in Arabidopsis mutant (Atnoa1) plants with impaired in vivo NO synthase activity, and in wild-type plants as well, 15) but simultaneous increases in NO and H 2 O 2 in tobacco cells induce apoptosis-like cell death. 20) In BY-2 cells, proline and betaine did not reduce NO production under either short-term or long-term NaCl treatment ( Fig. 3A and B), although both compounds suppress H 2 O 2 accumulation (Fig.…”

“…1,[12][13][14][15][16][17][18] Excess production of H 2 O 2 , O 2 À , and NO is toxic to plants, and causes oxidative damage to cellular constituents, leading to cell death. [12][13][14][18][19][20] In plant cells, salinity also leads to the accumulation of methylglyoxal (MG), a cytotoxic compound that can react with and modify other molecules, including DNA and proteins. [21][22][23] Because of the highly cytotoxic and reactive properties of H 2 O 2 , O 2 À , NO, and MG, their concentrations must be kept under strict control.…”

Study of interaction effect between triacontanol and nitric oxide on alleviating of oxidative stress arsenic toxicity in coriander seedlings

“…In a study with tobacco bright-yellow 2 cells, only the combined application of NO and ROS generators caused a remarkable increase in PAL activity. Both ROS and NO may stimulate expression of the pal gene (De Pinto et al 2002). In addition, Durner et al (1998) reported that NO induced activation of PAL gene (pal) expression and PAL enzyme activity in tobacco.…”

Differential generation of hydrogen peroxide upon exposure to zinc and cadmium in the hyperaccumulating plant specie (Sedum alfredii Hance)

“…The action of H 2 O 2 in stress resistance of plants was involved in many regulation processes (Baysal et al, 2007;Bright et al, 2006;de Pinto et al, 2002;Shin and Schachtman, 2004 (Fig.3). The content of H 2 O 2 with Zn 2+ treatment was much higher than that with Cd 2+ treatment.…”