Evidence map›Paper›PMID 17031387›Full record

ArticleBritish journal of pharmacology2006

Iron is not involved in oxidative stress-mediated cytotoxicity of doxorubicin and bleomycin.

H Kaiserová, G J M den Hartog, T Simůnek, L Schröterová, E Kvasnicková, A Bast

Abstract read
In one paragraph

Article in British journal of pharmacology, 2006. 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
–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

16 citing papers in PubMed.

  1. Article
  2. Review
  3. Modulating effect of vitamin D3 on the mutagenicity and carcinogenicity of doxorubicin in Drosophila melanogaster and in silico studies.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2020
    Article
  4. Liver damage in bleomycin-induced pulmonary fibrosis in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2019
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Inhibition of pancreatic tumoral cells by snake venom disintegrins.Toxicon : official journal of the International Society on Toxinology · 2015
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Cardiac toxicity: old and new issues in anti-cancer drugs.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2008
    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

6 authors.

H KaiserováDepartment of Biochemical Sciences, Charles University in Prague, Hradec Králové, Czech Republic. Helena.Kaiserova@faf.cuni.cz
G J M den Hartog
T Simůnek
L Schröterová
E Kvasnicková
A Bast

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeThe anticancer drugs doxorubicin and bleomycin are well-known for their oxidative stress-mediated side effects in heart and lung, respectively. It is frequently suggested that iron is involved in doxorubicin and bleomycin toxicity. We set out to elucidate whether iron chelation prevents the oxidative stress-mediated toxicity of doxorubicin and bleomycin and whether it affects their antiproliferative/proapoptotic effects. EXPERIMENTAL APPROACH: Cell culture experiments were performed in A549 cells. Formation of hydroxyl radicals was measured in vitro by electron paramagnetic resonance (EPR). We investigated interactions between five iron chelators and the oxidative stress-inducing agents (doxorubicin, bleomycin and H(2)O(2)) by quantifying oxidative stress and cellular damage as TBARS formation, glutathione (GSH) consumption and lactic dehydrogenase (LDH) leakage. The antitumour/proapoptotic effects of doxorubicin and bleomycin were assessed by cell proliferation and caspase-3 activity assay. KEY

resultsAll the tested chelators, except for monohydroxyethylrutoside (monoHER), prevented hydroxyl radical formation induced by H(2)O(2)/Fe(2+) in EPR studies. However, only salicylaldehyde isonicotinoyl hydrazone and deferoxamine protected intact A549 cells against H(2)O(2)/Fe(2+). Conversely, the chelators that decreased doxorubicin and bleomycin-induced oxidative stress and cellular damage (dexrazoxane, monoHER) were not able to protect against H(2)O(2)/Fe(2+). CONCLUSIONS AND IMPLICATIONS: We have shown that the ability to chelate iron as such is not the sole determinant of a compound protecting against doxorubicin or bleomycin-induced cytotoxicity. Our data challenge the putative role of iron and hydroxyl radicals in the oxidative stress-mediated cytotoxicity of doxorubicin and bleomycin and have implications for the development of new compounds to protects against this toxicity.

Indexed as

AldehydesAntibiotics, AntineoplasticApoptosisBleomycinCell Line, TumorCell ProliferationCell SurvivalDeferoxamineDoxorubicinElectron Spin Resonance SpectroscopyFree RadicalsHumansHydrazonesHydrogen PeroxideIronIron Chelating AgentsAldehydesAntibiotics, AntineoplasticBleomycinDeferoxamineDoxorubicinFenton's reagentFree RadicalsHydrazonesHydrogen PeroxideIronIron Chelating AgentsIron CompoundsIsoniazidPyridoxalpyridoxal isonicotinoyl hydrazoneRazoxanesalicylaldehyde isonicotinoyl hydrazone

Identifiers

PMID17031387
PMCPMC2014688

What OpenQuestion holds

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Registered trials

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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.