Evidence map›Paper›PMID 28553767›Full record

ArticleThe Journal of international medical research2017

Assessment of aflatoxin B1 myocardial toxicity in rats: mitochondrial damage and cellular apoptosis in cardiomyocytes induced by aflatoxin B1.

Junhua Ge, Haichu Yu, Jian Li, Zhexun Lian, Hongjing Zhang, Hao Fang, Lusha Qian

Open access · goldAbstract read
In one paragraph

Article in The Journal of international medical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
5.6field-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

13 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  3. Protective effect of Zhizi Huangqi Shanzha formula on aflatoxin poisoning in mice and its effect on intestinal flora.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024
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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

7 authors at 2 institutions in 1 country.

Junhua GeDepartment of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China.
Haichu YuDepartment of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China.
Jian LiDepartment of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China.
Zhexun LianDepartment of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China.
Hongjing ZhangDepartment of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China.
Hao FangDepartment of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China.
Lusha QianDepartment of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, China.
Affiliated Hospital of Qingdao University · CNQingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective The number of deaths from heart disease is increasing worldwide. Aflatoxin B1 (AFB1), a toxin produced by the fungi Aspergillus flavus and Aspergillus parasiticus, is frequently detected in improperly processed/stored human food products. While AFB1 hepatotoxicity and carcinogenic properties have been well addressed, its myocardial toxicity is poorly documented. This study aimed to investigate myocardial toxic activity of AFB1. Methods Ten rats were fed with AFB1 at a dose that did not result in acute toxic reactions for 30 days and 10 vehicle-fed rats served as controls. Transmission electron microscopy was used to assess mitochondrial damage in cardiomyocytes. The terminal deoxynucleotidyl transferase-mediated UTP nick-end labelling assay was performed to detect apoptosis of cardiomyocytes. Western blotting was performed to measure apoptotic proteins (i.e., active caspase-3, Bax, and Bcl-2) in heart tissue. Results AFB1 treatment resulted in mitochondrial membrane disruption and disorganization of cristae, which are indicators of mitochondrial damage. Myocardial cell apoptosis was significantly higher after AFB1 treatment (22.07% ± 3.29%) compared with controls (6.27% ± 2.78%, P < 0.05). AFB1 treatment enhanced expression of active caspase-3, Bax, and Bcl-2 in cardiac tissue. Conclusion Various adverse effects are exerted by AFB1 on the heart, indicating AFB1 myocardial toxicity.

Indexed as

Aflatoxin B1AnimalsApoptosisCaspase 3FemaleHeartMicroscopy, Electron, ScanningMitochondria, HeartMyocytes, CardiacProto-Oncogene Proteins c-bcl-2RatsRats, Sprague-DawleyAflatoxin B1Caspase 3Proto-Oncogene Proteins c-bcl-2Aflatoxin B1Bcl-2caspase-3cell apoptosismitochondriamyocardial toxicity

Identifiers

PMID28553767
PMCPMC5536410
OpenAlexW2617912275

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.