Evidence map›Paper›PMID 19236887›Full record

ReviewToxicology and applied pharmacology2009

Role of oxidative stress in cadmium toxicity and carcinogenesis.

Jie Liu, Wei Qu, Maria B Kadiiska

Abstract readReview
In one paragraph

Review in Toxicology and applied pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 238 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
238citing papers in PubMed, 1 pooled it
31.2field-weighted citation impact, top 1% 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

238 citing papers in PubMed, 1 synthesis or guideline pooled it, 837 citations in OpenAlex.

  1. Pooled it
  2. Nifuroxazide Pretreatment Protects Against Acute CdClAntioxidants (Basel, Switzerland) · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. The RNA mPlant biotechnology journal · 2026
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Alpha-lipoic acid, as an effective agent against toxic elements: a review.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review

178 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Jie LiuInorganic Carcinogenesis Section, Laboratory of Comparative Carcinogenesis, NCI at NIEHS, Research Triangle Park, NC 27709, USA. Liu6@niehs.nih.gov
Wei Qu
Maria B Kadiiska
National Institute of Environmental Health Sciences · USNational Institutes of Health · USResearch Triangle Park Foundation · US

Funding

Intramural NIH HHS NIH0011069698
6 · The paper itself

Abstract

Cadmium (Cd) is a toxic metal, targeting the lung, liver, kidney, and testes following acute intoxication, and causing nephrotoxicity, immunotoxicity, osteotoxicity and tumors after prolonged exposures. Reactive oxygen species (ROS) are often implicated in Cd toxicology. This minireview focused on direct evidence for the generation of free radicals in intact animals following acute Cd overload and discussed the association of ROS in chronic Cd toxicity and carcinogenesis. Cd-generated superoxide anion, hydrogen peroxide, and hydroxyl radicals in vivo have been detected by the electron spin resonance spectra, which are often accompanied by activation of redox sensitive transcription factors (e.g., NF-kappaB, AP-1 and Nrf2) and alteration of ROS-related gene expression. It is generally agreed upon that oxidative stress plays important roles in acute Cd poisoning. However, following long-term Cd exposure at environmentally-relevant low levels, direct evidence for oxidative stress is often obscure. Alterations in ROS-related gene expression during chronic exposures are also less significant compared to acute Cd poisoning. This is probably due to induced adaptation mechanisms (e.g., metallothionein and glutathione) following chronic Cd exposures, which in turn diminish Cd-induced oxidative stress. In chronic Cd-transformed cells, less ROS signals are detected with fluorescence probes. Acquired apoptotic tolerance renders damaged cells to proliferate with inherent oxidative DNA lesions, potentially leading to tumorigenesis. Thus, ROS are generated following acute Cd overload and play important roles in tissue damage. Adaptation to chronic Cd exposure reduces ROS production, but acquired Cd tolerance with aberrant gene expression plays important roles in chronic Cd toxicity and carcinogenesis.

Indexed as

Adaptation, PhysiologicalAnimalsApoptosisBone DiseasesCadmiumCell Transformation, NeoplasticDNA DamageDose-Response Relationship, DrugElectron Spin Resonance SpectroscopyEnvironmental PollutantsGene Expression Regulation, NeoplasticHumansKidney DiseasesNeoplasmsOxidative StressReactive Oxygen SpeciesCadmiumEnvironmental PollutantsReactive Oxygen Species

Identifiers

PMID19236887
PMCPMC4287357
OpenAlexW2025369275

What OpenQuestion holds

Textmetadata
LicenceTDM
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.