ArticleMolecular neurobiology2025
Neurotoxic Effects of Atrazine on Dopaminergic System via miRNAs and Energy-Sensing Pathways.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
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Who cites it
3 citing papers in PubMed.
- Developmental neurotoxicity of atrazine: decreased synaptic spine density and miRNA-driven GluN2A downregulation in primary hippocampal neurons.Archives of toxicology · 2026Article
- Gestational and Lactational Atrazine Exposure Potentially Mediates Behavioral and Dopaminergic Alterations in Rat Offspring: Insights into Nurr1-Related ceRNA Regulation.International journal of molecular sciences · 2026Article
- Epigenetic and Genotoxic Mechanisms of PFAS-Induced Neurotoxicity: A Molecular and Transgenerational Perspective.Toxics · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atrazine (ATR, 2-chloro-4-ethylamino-6-isopropylamino-1,3,5-triazine) is a globally prevalent herbicide known to induce dopaminergic neurotoxicity at high concentrations. MicroRNAs (miRNAs), pivotal in regulating gene expression post-transcriptionally, play essential roles in neuronal differentiation, proliferation, and apoptosis. This study investigates the effects of ATR on the dopaminergic system and behavioral responses in rats, with a particular focus on critical dopaminergic proteins such as tyrosine hydroxylase (TH), nuclear receptor related-1 protein (NURR1), and α-synuclein. The results reveal that ATR exposure significantly reduces the expression of TH and NURR1, while elevating levels of α-synuclein. Through miRNA sequencing and proteomic analysis, we identify alterations in miRNA and protein profiles that are intricately linked to the development of the dopaminergic system. Notably, treatment with ATR results in a marked increase in AMPK levels concurrent with a decrease in miR-322-5p. The differentially expressed genes associated with ATR exposure primarily influence the dopaminergic system by engaging in critical pathways such as AMPK, mTOR, autophagy, FoxO, and HIPPO. This study underscores the neurotoxic impact of ATR on the dopaminergic system via miRNA regulatory mechanisms and energy-sensing pathways, including AMPK and SIRT1, providing a molecular foundation for developing strategies to prevent and treat neurotoxicity induced by ATR exposure.
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Registered trials
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.