Evidence map›Paper›PMID 41193730›Full record

ArticleScientific reports2025

Exploring the mechanism of methyl parathion and its degradation product on depression through network toxicology and molecular docking.

Min Cao, Bin-Bin Fan, Lun-Shan Xu, Jiao Xu, Yi-Hua Zhang

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

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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

1 citing paper in PubMed.

  1. 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

5 authors.

Min CaoDepartment of Neurosurgery, Daping Hospital, Army Medical University, Chongqing, China.
Bin-Bin FanDepartment of Neurosurgery, Daping Hospital, Army Medical University, Chongqing, China.
Lun-Shan XuDepartment of Neurosurgery, Daping Hospital, Army Medical University, Chongqing, China.
Jiao XuDepartment of Neurosurgery, Daping Hospital, Army Medical University, Chongqing, China. xujiao@tmmu.edu.cn.
Yi-Hua ZhangDepartment of Neurosurgery, Daping Hospital, Army Medical University, Chongqing, China. zhangyihua666@tmmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methyl parathion and its degradation product p-nitrophenol have become important environmental problems due to their high toxicity and persistence. In this study, the toxicological mechanism of methyl parathion and p-nitrophenol exposure increasing the risk of depression was studied through network toxicology and molecular docking methods. Based on the comprehensive analysis of PharmMapper, STITCH, SwissTargetPrediction, Similarity ensemble approach (SEA) and GeneCards databases, 35 potential targets related to methyl parathion and p-nitrophenol exposure were identified. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed the key pathways of methyl parathion and p-nitrophenol affecting depression, included insulin-like growth factor receptor signaling pathway, serotonergic synapse. Combined with protein-protein interaction (PPI) network analysis and KEGG analysis, 14 core targets of depression related to methyl parathion and p-nitrophenol were screened out. Further, the targets MAP2K1 and APP with the highest binding scores with methyl parathion and p-nitrophenol, respectively, were screened by DeepPurpose, and the common target HRAS for molecular docking was determined. The molecular docking analysis further verified that methyl parathion and p-nitrophenol may have good binding activity with HRAS. This study provides valuable insights for understanding the molecular mechanism of environmental pollutants methyl parathion and p-nitrophenol affecting depression, and provides a theoretical basis for understanding the health risks of methyl parathion and p-nitrophenol.

Indexed as

DepressionMethyl ParathionMolecular Docking SimulationNitrophenolsHumansProtein Interaction Maps4-nitrophenolMethyl ParathionNitrophenolsDepressionMethyl parathionMolecular dockingNetwork toxicologyp-nitrophenol

Identifiers

PMID41193730
PMCPMC12589578

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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.