Evidence map›Paper›PMID 26225731›Full record

ArticleRedox biology2015

Singlet oxygen treatment of tumor cells triggers extracellular singlet oxygen generation, catalase inactivation and reactivation of intercellular apoptosis-inducing signaling.

Michaela Riethmüller, Nils Burger, Georg Bauer

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Review
  3. Alkyl-π Liquids as Condensed-State Singlet Oxygen Photosensitizers.Chemistry (Weinheim an der Bergstrasse, Germany) · 2025
    Article
  4. Article
  5. Article
  6. Generation of singlet oxygen inside living cells: correlation between phosphorescence decay lifetime, localization and outcome of photodynamic action.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2024
    Article
  7. Review
  8. Review
  9. Cellular Mechanisms of Singlet Oxygen in Photodynamic Therapy.International journal of molecular sciences · 2023
    Review
  10. Article
  11. Review
  12. Role of photobleaching process of indocyanine green for killing neuroblastoma cells.Biochemical and biophysical research communications · 2022
    Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Michaela RiethmüllerInstitute of Virology, Department of Medical Microbiology and Hygiene, University Medical Center, Freiburg, Germany.
Nils BurgerInstitute of Virology, Department of Medical Microbiology and Hygiene, University Medical Center, Freiburg, Germany.
Georg BauerInstitute of Virology, Department of Medical Microbiology and Hygiene, University Medical Center, Freiburg, Germany. Electronic address: georg.bauer@uniklinik-freiburg.de.
Institute of Medical Microbiology and Hygiene · DEUniversity Medical Center Freiburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intracellular singlet oxygen generation in photofrin-loaded cells caused cell death without discrimination between nonmalignant and malignant cells. In contrast, extracellular singlet oxygen generation caused apoptosis induction selectively in tumor cells through singlet oxygen-mediated inactivation of tumor cell protective catalase and subsequent reactivation of intercellular ROS-mediated apoptosis signaling through the HOCl and the NO/peroxynitrite signaling pathway. Singlet oxygen generation by extracellular photofrin alone was, however, not sufficient for optimal direct inactivation of catalase, but needed to trigger the generation of cell-derived extracellular singlet oxygen through the interaction between H2O2 and peroxynitrite. Thereby, formation of peroxynitrous acid, generation of hydroxyl radicals and formation of perhydroxyl radicals (HO2(.)) through hydroxyl radical/H2O2 interaction seemed to be required as intermediate steps. This amplificatory mechanism led to the formation of singlet oxygen at a sufficiently high concentration for optimal inactivation of membrane-associated catalase. At low initial concentrations of singlet oxygen, an additional amplification step needed to be activated. It depended on singlet oxygen-dependent activation of the FAS receptor and caspase-8, followed by caspase-8-mediated enhancement of NOX activity. The biochemical mechanisms described here might be considered as promising principle for the development of novel approaches in tumor therapy that specifically direct membrane-associated catalase of tumor cells and thus utilize tumor cell-specific apoptosis-inducing ROS signaling.

Indexed as

Gene Expression Regulation, NeoplasticSignal TransductionAnimalsApoptosisCaspase 8CatalaseCell LineCell Line, TumorDihematoporphyrin EtherEnzyme Inhibitorsfas ReceptorFibroblastsHumansHydrogen PeroxideHypochlorous AcidLight4-(2-aminoethyl)benzenesulfonylfluoride5,10,15,20-tetrakis(4-sulfonatophenyl)porphyrinato iron(III) chlorideCASP8 protein, humanCaspase 8CatalaseDihematoporphyrin EtherEnzyme Inhibitorsfas ReceptorHydrogen PeroxideHypochlorous AcidMetalloporphyrinsNADPH OxidasesNitric OxidePeroxynitrous AcidPhotosensitizing AgentsSinglet OxygenSulfonesTaurineCatalaseIntercellular apoptosis-inducing signalingNitric oxidePeroxnitritePhotodynamic therapySinglet oxygen

Identifiers

PMID26225731
PMCPMC4532730
OpenAlexW1008539174

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.