Evidence map›Paper›PMID 12835108›Full record

ArticleNeurotoxicity research1999

Management of oxidative stress in the CNS: the many roles of glutathione.

B H Juurlink

Abstract read
PubMed Publisher
In one paragraph

Article in Neurotoxicity research, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Carbonyl stress induces hypertension and cardio-renal vascular injury in Dahl salt-sensitive rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2013
    Article
  5. Article
  6. Article
  7. Dietary approach to attenuate oxidative stress, hypertension, and inflammation in the cardiovascular system.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  8. Review
  9. Article
  10. Article
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

1 author.

B H JuurlinkDepartment of Anatomy and Cell Biology, The Cameco Multiple Sclerosis and Neuroscience Research Centre, College of Medicine, University of Saskatchewan, 107 Wiggins Rd., Saskatoon, SK, S7N 5E5 Canada. juurlink@duke.usask.ca

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An outline is given of mechanisms that generate oxidative stress and inflammation. Considered are the metabolic mechanisms that give rise to peroxides, the source of strong oxidants; the production of dicarbonyls that interact with macromolecules to form advanced glycation endproducts; and the role that activation of the transcription factor NF(Kappa)B has in the expression of pro-inflammatory genes. Management of oxidative stress is considered by outlining the central role of reduced glutathione (GSH) in peroxide scavenging, dicarbonyl scavenging and activation of NF(Kappa)B. Cellular GSH levels are dictated by the balance between consumption, oxidation of GSH, reduction of oxidized-glutathione, and synthesis. The rate-limiting enzyme in GSH synthesis is L-gamma-glutamyl-L-cysteine synthase, a phase II enzyme. Phase II enzyme inducers are found in many fruits and vegetables. It is suggested that dietary phase II enzyme inducers be investigated for their potential for preventing or retarding the development of degenerative diseases that have an underlying oxidative stress and inflammatory component.

Identifiers

PMID12835108

What OpenQuestion holds

Textmetadata
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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.