Evidence map›Paper›PMID 27669300›Full record

ArticleToxins2016

Different Toxicity Mechanisms for Citrinin and Ochratoxin A Revealed by Transcriptomic Analysis in Yeast.

Elena Vanacloig-Pedros, Markus Proft, Amparo Pascual-Ahuir

Open access · goldAbstract read
In one paragraph

Article in Toxins, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
8.2field-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

15 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Mycotoxin Removal and Transcriptional Response ofFoods (Basel, Switzerland) · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Microbial detoxification of mycotoxins in food.Frontiers in microbiology · 2022
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Nutraceuticals: opening the debate for a regulatory framework.British journal of clinical pharmacology · 2018
    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.

Elena Vanacloig-PedrosDepartment of Biotechnology, Instituto de Biología Molecular y Celular de Plantas, Universidad Politécnica de Valencia, Ingeniero Fausto Elio s/n, 46022 Valencia, Spain. mevaped@etsia.upv.es.
Markus ProftDepartment of Molecular and Cellular Pathology and Therapy, Instituto de Biomedicina de Valencia IBV-CSIC, Jaime Roig 11, 46010 Valencia, Spain. mproft@ibv.csic.es.
Amparo Pascual-AhuirDepartment of Biotechnology, Instituto de Biología Molecular y Celular de Plantas, Universidad Politécnica de Valencia, Ingeniero Fausto Elio s/n, 46022 Valencia, Spain. apascual@ibmcp.upv.es.
Instituto de Biología Molecular y Celular de Plantas · ESInstituto de Biomedicina de Valencia · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Citrinin (CIT) and ochratoxin A (OTA) are important mycotoxins, which frequently co-contaminate foodstuff. In order to assess the toxicologic threat posed by the two mycotoxins separately or in combination, their biological effects were studied here using genomic transcription profiling and specific live cell gene expression reporters in yeast cells. Both CIT and OTA cause highly transient transcriptional activation of different stress genes, which is greatly enhanced by the disruption of the multidrug exporter Pdr5. Therefore, we performed genome-wide transcription profiling experiments with the pdr5 mutant in response to acute CIT, OTA, or combined CIT/OTA exposure. We found that CIT and OTA activate divergent and largely nonoverlapping gene sets in yeast. CIT mainly caused the rapid induction of antioxidant and drug extrusion-related gene functions, while OTA mainly deregulated developmental genes related with yeast sporulation and sexual reproduction, having only a minor effect on the antioxidant response. The simultaneous exposure to CIT and OTA gave rise to a genomic response, which combined the specific features of the separated mycotoxin treatments. The application of stress-specific mutants and reporter gene fusions further confirmed that both mycotoxins have divergent biological effects in cells. Our results indicate that CIT exposure causes a strong oxidative stress, which triggers a massive transcriptional antioxidant and drug extrusion response, while OTA mainly deregulates developmental genes and only marginally induces the antioxidant defense.

Indexed as

CitrininGene Expression ProfilingOchratoxinsOxidative StressOxidoreductasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSuperoxide DismutaseSuperoxide Dismutase 2CitrininGRE2 protein, S cerevisiaeochratoxin AOchratoxinsOxidoreductasesSaccharomyces cerevisiae ProteinsSuperoxide DismutaseSuperoxide Dismutase 2Citrinindose responsemycotoxinsOchratoxin Aoxidative stressSaccharomyces cerevisiaeTranscriptome

Identifiers

PMID27669300
PMCPMC5086634
OpenAlexW2521796303

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.