Evidence map›Paper›PMID 24623797›Full record

ReviewThe Journal of endocrinology2014

Oxidative stress and adrenocortical insufficiency.

R Prasad, J C Kowalczyk, E Meimaridou, H L Storr, L A Metherell

Open access · hybridAbstract readReview
In one paragraph

Review in The Journal of endocrinology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

35 citing papers in PubMed, 67 citations in OpenAlex.

  1. Trial
  2. The essential role of the redox balance in adrenal steroidogenesis.Archives of endocrinology and metabolism · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Mitomycin C-induced DNA double-strand breaks are enhanced by catalytical inactivation of DNA polymerase κ in mice.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Easily misdiagnosed X-linked adrenoleukodystrophy.Italian journal of pediatrics · 2024
    Article
  12. Article
  13. Article
  14. Inflammation-induced adrenal dysfunction.Nature reviews. Endocrinology · 2023
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Adrenal Dysfunction in Mitochondrial Diseases.International journal of molecular sciences · 2023
    Review
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

5 authors at 1 institution in 1 country.

R PrasadBarts and the London School of Medicine and DentistryWilliam Harvey Research Institute, Centre for Endocrinology, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK.
J C KowalczykBarts and the London School of Medicine and DentistryWilliam Harvey Research Institute, Centre for Endocrinology, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK.
E MeimaridouBarts and the London School of Medicine and DentistryWilliam Harvey Research Institute, Centre for Endocrinology, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK.
H L StorrBarts and the London School of Medicine and DentistryWilliam Harvey Research Institute, Centre for Endocrinology, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK.
L A MetherellBarts and the London School of Medicine and DentistryWilliam Harvey Research Institute, Centre for Endocrinology, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London EC1M 6BQ, UK l.a.metherell@qmul.ac.uk.
Queen Mary University of London · GB

Funding

Medical Research Council G0801265Medical Research Council MR/K020455/1Wellcome Trust WT095984AIA
6 · The paper itself

Abstract

Maintenance of redox balance is essential for normal cellular functions. Any perturbation in this balance due to increased reactive oxygen species (ROS) leads to oxidative stress and may lead to cell dysfunction/damage/death. Mitochondria are responsible for the majority of cellular ROS production secondary to electron leakage as a consequence of respiration. Furthermore, electron leakage by the cytochrome P450 enzymes may render steroidogenic tissues acutely vulnerable to redox imbalance. The adrenal cortex, in particular, is well supplied with both enzymatic (glutathione peroxidases and peroxiredoxins) and non-enzymatic (vitamins A, C and E) antioxidants to cope with this increased production of ROS due to steroidogenesis. Nonetheless oxidative stress is implicated in several potentially lethal adrenal disorders including X-linked adrenoleukodystrophy, triple A syndrome and most recently familial glucocorticoid deficiency. The finding of mutations in antioxidant defence genes in the latter two conditions highlights how disturbances in redox homeostasis may have an effect on adrenal steroidogenesis.

Indexed as

Oxidative StressAdrenal InsufficiencyAntioxidantsHumansMitochondriaModels, BiologicalOxidation-ReductionReactive Oxygen SpeciesAntioxidantsReactive Oxygen Speciesadrenal insufficiencyoxidative stressreactive oxygen speciessteroidogenesis

Identifiers

PMID24623797
PMCPMC4045218
OpenAlexW2126797871

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.