Evidence map›Paper›PMID 32424756›Full record

ReviewEnvironmental science and pollution research international2020

Ochratoxin A-induced genotoxic and epigenetic mechanisms lead to Alzheimer disease: its modulation with strategies.

Kamal Niaz, Syed Zahid Ali Shah, Fazlullah Khan, Mohammed Bule

Abstract readReview
PubMed Publisher
In one paragraph

Review in Environmental science and pollution research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 5% 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, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  11. TheAntioxidants (Basel, Switzerland) · 2022
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  16. Environmental pollutants and the risk of neurological disorders.Environmental science and pollution research international · 2020
    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 3 countries.

Kamal NiazDepartment of Pharmacology and Toxicology, Faculty of Bio-Sciences, Cholistan University of Veterinary and Animal Sciences, Bahawalpur, 63100, Pakistan. kamalniaz1989@gmail.com.ORCID http://orcid.org/0000-0001-8670-4356
Syed Zahid Ali ShahDepartment of Pathology, Faculty of Veterinary Science, Cholistan University of Veterinary and Animal Sciences, Bahawalpur, 63100, Pakistan.
Fazlullah KhanThe Institute of Pharmaceutical Sciences (TIPS), School of Pharmacy, International Campus, Tehran University of Medical Sciences (IC-TUMS), Tehran, 1417614411, Iran.
Mohammed BuleDepartment of Pharmacy, College of Medicine and Health Sciences, Ambo University, Ambo, Oromia, Ethiopia.
University of Veterinary and Animal Sciences · PKAmbo University · ETTehran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ochratoxin A (OTA) is a naturally occurring mycotoxin mostly found in food items including grains and coffee beans. It induces DNA single-strand breaks and has been considered to be carcinogenic. It is recognized as a serious threat to reproductive health both in males and females. OTA is highly nephrotoxic and carcinogenic, and its potency changes evidently between species and sexes. There is a close association between OTA, mutagenicity, carcinogenicity, and genotoxicity, but the underlying mechanisms are not clear. Reports regarding genotoxic effects in relation to OTA which leads to the induction of DNA adduct formation, protein synthesis inhibition, perturbation of cellular energy production, initiation of oxidative stress, induction of apoptosis, influences on mitosis, induction of cell cycle arrest, and interference with cytokine pathways. All these mechanisms are associated with nephrotoxicity, hepatotoxicity, teratotoxicity, immunological toxicity, and neurotoxicity. OTA administration activates various mechanisms such as p38 MAPK, JNKs, and ERKs dysfunctions, BDNF disruption, TH overexpression, caspase-3 and 9 activation, and ERK-1/2 phosphorylation which ultimately lead to Alzheimer disease (AD) progression. The current review will focus on OTA in terms of recent discoveries in the field of molecular biology. The main aim is to investigate the underlying mechanisms of OTA in regard to genotoxicity and epigenetic modulations that lead to AD. Also, we will highlight the strategies for the purpose of attenuating the hazards posed by OTA exposure.

Indexed as

Alzheimer DiseaseOchratoxinsDNA DamageEpigenesis, GeneticFemaleHumansMaleochratoxin AOchratoxinsAlzheimer diseaseDNA methylationEpigeneticsGenotoxicityHistone modificationsNephrotoxicityOchratoxin ATherapeutics

Identifiers

PMID32424756
OpenAlexW3028363133

What OpenQuestion holds

Textmetadata
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.