Evidence map›Paper›PMID 28737676›Full record

ArticleAntioxidants (Basel, Switzerland)2017

High Dose Ascorbate Causes Both Genotoxic and Metabolic Stress in Glioma Cells.

Maria Leticia Castro, Georgia M Carson, Melanie J McConnell, Patries M Herst

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Glioblastoma Metabolism: Insights and Therapeutic Strategies.International journal of molecular sciences · 2023
    Review
  4. Review
  5. Article
  6. Frontiers in microbiology · 2022
    Article
  7. High-dose intravenous vitamin C, a promising multi-targeting agent in the treatment of cancer.Journal of experimental & clinical cancer research : CR · 2021
    Review
  8. Article
  9. TET3 regulates DNA hydroxymethylation of neuroprotective genes following focal ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. 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

4 authors at 3 institutions in 1 country.

Maria Leticia CastroSchool of Biological Sciences, Victoria University, P.O.Box 600, Wellington 6140, New Zealand. leticia.castro@vuw.ac.nz.
Georgia M CarsonSchool of Biological Sciences, Victoria University, P.O.Box 600, Wellington 6140, New Zealand. georgia.carson@hotmail.co.nz.
Melanie J McConnellSchool of Biological Sciences, Victoria University, P.O.Box 600, Wellington 6140, New Zealand. Melanie.McConnell@vuw.ac.nz.
Patries M HerstMalaghan Institute of Medical Research, P.O.Box 7060, Wellington 6242, New Zealand. patries.herst@otago.ac.nz.
Victoria University of Wellington · NZMalaghan Institute of Medical Research · NZUniversity of Otago · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have previously shown that exposure to high dose ascorbate causes double stranded breaks (DSBs) and a build-up in S-phase in glioblastoma (GBM) cell lines. Here we investigated whether or not this was due to genotoxic stress as well as metabolic stress generated by exposure to high dose ascorbate, radiation, ascorbate plus radiation and H₂O₂ in established and primary GBM cell lines. Genotoxic stress was measured as phosphorylation of the variant histone protein, H2AX, 8-oxo-7,8-dihydroguanine (8OH-dG) positive cells and cells with comet tails. Metabolic stress was measured as a decrease in NADH flux, mitochondrial membrane potential (by CMXRos), ATP levels (by ATP luminescence) and mitochondrial superoxide production (by mitoSOX). High dose ascorbate, ascorbate plus radiation, and H₂O₂ treatments induced both genotoxic and metabolic stress. Exposure to high dose ascorbate blocked DNA synthesis in both DNA damaged and undamaged cell of ascorbate sensitive GBM cell lines. H₂O₂ treatment blocked DNA synthesis in all cell lines with and without DNA damage. DNA synthesis arrest in cells with damaged DNA is likely due to both genotoxic and metabolic stress. However, arrest in DNA synthesis in cells with undamaged DNA is likely due to oxidative damage to components of the mitochondrial energy metabolism pathway.

Indexed as

DNA synthesis arrestgenotoxic stressH2O2high dose ascorbatemetabolic stressoxidative stressradiation

Identifiers

PMID28737676
PMCPMC5618086
OpenAlexW2737013379

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.