Evidence map›Paper›PMID 32488703›Full record

ArticleEnvironmental science and pollution research international2020

Over-gene expression in the apoptotic, oxidative damage and liver injure in female rats exposed to butralin.

Amel A Refaie, Amal Ramadan, Nevien M Sabry, Wagdy K B Khalil, Abdel-Tawab H Mossa

Abstract read
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In one paragraph

Article 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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 28 citations in OpenAlex.

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  9. Antioxidants (Basel, Switzerland) · 2021
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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

5 authors at 1 institution in 1 country.

Amel A RefaieEnvironmental Toxicology Research Unit (ETRU), Pesticide Chemistry Department, Chemical Industries Research Division, National Research Centre (NRC), P.O. 12622, 33 El Bohouth Street (former El Tahrir St.), Dokki, Giza, Egypt.
Amal RamadanDepartment of Biochemistry, Genetic Engineering & Biotechnology Research Division, National Research Centre (NRC), P.O. 12622, 33 El Bohouth Street (former El Tahrir St.), Dokki, Giza, Egypt.
Nevien M SabryDepartment of Cell Biology, National Research Centre (NRC), P.O. 12622, 33 El Bohouth Street (former El Tahrir St.), Dokki, Giza, Egypt.
Wagdy K B KhalilDepartment of Cell Biology, National Research Centre (NRC), P.O. 12622, 33 El Bohouth Street (former El Tahrir St.), Dokki, Giza, Egypt.
Abdel-Tawab H MossaEnvironmental Toxicology Research Unit (ETRU), Pesticide Chemistry Department, Chemical Industries Research Division, National Research Centre (NRC), P.O. 12622, 33 El Bohouth Street (former El Tahrir St.), Dokki, Giza, Egypt. abdeltawab.mossa@yahoo.com.ORCID http://orcid.org/0000-0002-8112-8553
National Research Centre · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study is the first report for studying the toxic effects of butralin herbicide on COX2, BAX, and Bcl2 gene expression, oxidative stress, and liver damage in female rats. Female rats were received butralin in drinking water for 28 days at concentration 4.16, 312, and 3120 mg/L that corresponded to the acceptable daily intake (ADI), no observed adverse effect level (NOAEL), and 10 NOAEL, respectively. Butralin decreased body weights and increased relative liver weight of female rats exposed to high dose. It caused significant elevation in liver function enzymes, lipid peroxidation, and reactive oxygen species (ROS). Antioxidant enzymes were decreased in liver tissue by increasing the dose. Butralin induced over-expression in the apoptotic related genes including COX2, BAX, and Bcl2 and pathological alteration in the liver of female rats especially at a high dose. It can be concluded that butralin induced oxidative damage and liver injure. The mechanism of damage could be due to generate reactive oxygen species, and increase lipid peroxidation that causes over-expression in the apoptotic related genes including COX2, BAX, and Bcl2. From the Benchmark dose (BMD) approach, there is dose-dependent manner in body weight, AST, ALT, and ALP, and ALT is a very sensitive parameter.

Indexed as

Lipid PeroxidationLiverAniline CompoundsAnimalsAntioxidantsFemaleOxidative StressRatsRats, WistarAniline CompoundsAntioxidantsbutralinButralinGene expressionHerbicideLiverOxidative stressRatsReactive oxygen species

Identifiers

PMID32488703
OpenAlexW3029699103

What OpenQuestion holds

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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.