Evidence map›Paper›PMID 12376637›Full record

ArticlePlant physiology2002

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.

Maria Concetta de Pinto, Franca Tommasi, Laura De Gara

Open access · greenAbstract read
In one paragraph

Article in Plant physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
24.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 260 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
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  7. Article
  8. Article
  9. Vitamin C in Plants: From Functions to Biofortification.Antioxidants (Basel, Switzerland) · 2019
    Review
  10. Article
  11. Elevated COProtoplasma · 2019
    Article
  12. Article
  13. HFrontiers in plant science · 2018
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Maria Concetta de PintoDipartimento di Biologia e Patologia Vegetale, Via E. Orabona 4, I-70125 Bari, Italy.
Franca Tommasi
Laura De Gara
Centro di Ricerca per la Patologia Vegetale · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AntioxidantsApoptosisAscorbate PeroxidasesAscorbic AcidCell LineCells, CulturedGlucoseGlucose OxidaseGlutathioneGlutathione DisulfideGlutathione ReductaseHydrogen PeroxideImmunity, InnateLipid PeroxidationNADH, NADPH OxidoreductasesNicotianaAntioxidantsAscorbate PeroxidasesAscorbic AcidGlucoseGlucose OxidaseGlutathioneglutathione dehydrogenase (ascorbate)Glutathione DisulfideGlutathione ReductaseHydrogen Peroxidemonodehydroascorbate reductase (NADH)NADH, NADPH OxidoreductasesNitric OxideNitroprussideOxidoreductasesPeroxidasesPhenylalanine Ammonia-LyaseReactive Oxygen Species

Identifiers

PMID12376637
PMCPMC166599
OpenAlexW2169831209

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.