Evidence map›Paper›PMID 36563536›Full record

ReviewRedox biology2023

The good Samaritan glutathione-S-transferase P1: An evolving relationship in nitric oxide metabolism mediated by the direct interactions between multiple effector molecules.

Tiffany M Russell, Des R Richardson

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Acrylamide Neurotoxicity Studies inAntioxidants (Basel, Switzerland) · 2025
    Article
  7. Genes · 2025
    Review
  8. Magnolol Inhibits the Growth ofThe Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2025
    Article
  9. Article
  10. Anti-Neuroinflammatory Effect of Ombuin fromInternational journal of molecular sciences · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. The Role of Glutathione in Selected Viral Diseases.Antioxidants (Basel, Switzerland) · 2023
    Review
  16. Review
  17. 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

2 authors at 2 institutions in 2 countries.

Tiffany M RussellDepartment of Pathology and Biological Responses, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Des R RichardsonCentre for Cancer Cell Biology and Drug Discovery, Griffith Institute for Drug Discovery, Griffith University, Nathan, 4111, Australia. Electronic address: d.richardson@griffith.edu.au.
Griffith University · AUNagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glutathione-S-transferases (GSTs) are phase II detoxification isozymes that conjugate glutathione (GSH) to xenobiotics and also suppress redox stress. It was suggested that GSTs have evolved not to enhance their GSH affinity, but to better interact with and metabolize cytotoxic nitric oxide (NO). The interactions between NO and GSTs involve their ability to bind and store NO as dinitrosyl-dithiol iron complexes (DNICs) within cells. Additionally, the association of GSTP1 with inducible nitric oxide synthase (iNOS) results in its inhibition. The function of NO in vasodilation together with studies associating GSTM1 or GSTT1 null genotypes with preeclampsia, additionally suggests an intriguing connection between NO and GSTs. Furthermore, suppression of c-Jun N-terminal kinase (JNK) activity occurs upon increased levels of GSTP1 or NO that decreases transcription of JNK target genes such as c-Jun and c-Fos, which inhibit apoptosis. This latter effect is mediated by the direct association of GSTs with MAPK proteins. GSTP1 can also inhibit nuclear factor kappa B (NF-κB) signaling through its interactions with IKKβ and Iκα, resulting in decreased iNOS expression and the stimulation of apoptosis. It can be suggested that the inhibitory activity of GSTP1 within the JNK and NF-κB pathways may be involved in crosstalk between survival and apoptosis pathways and modulating NO-mediated ROS generation. These studies highlight an innovative role of GSTs in NO metabolism through their interaction with multiple effector proteins, with GSTP1 functioning as a "good Samaritan" within each pathway to promote favorable cellular conditions and NO levels.

Indexed as

NF-kappa BNitric OxideGlutathioneGlutathione S-Transferase piGlutathione TransferaseIronNitrogen Oxidesdinitrosyl iron complexGlutathioneGlutathione S-Transferase piGlutathione TransferaseIronNF-kappa BNitric OxideNitrogen OxidesDinitrosyl dithiol iron complexesGlutathione S-transferaseInducible nitric oxide synthaseJun N-terminal kinaseNF-κBNitric oxide

Identifiers

PMID36563536
PMCPMC9800640
OpenAlexW4311544071

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.