ArticleScientific reports2026
Organophosphate pesticide exerts toxic effect on the optic nerve of glaucoma rats by promoting oxidative stress and inflammation.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- The Eye as a Window to Neurodegeneration: Oxidative Stress, Optic Nerve Vulnerability, and Retinal Biomarkers-A Scoping Review.Antioxidants (Basel, Switzerland) · 2026Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glaucoma, a leading cause of irreversible blindness, involves progressive retinal ganglion cell (RGC) loss. Beyond intraocular pressure (IOP), environmental risk factors like pesticide exposure are increasingly implicated. Dimethyl phosphate (DMP), a key metabolite of organophosphorus pesticides, accumulates in the body and exhibits systemic toxicity. However, its direct role and mechanism in glaucoma pathogenesis remain entirely unexplored. We investigated the impact of DMP on glaucoma progression using a rat glaucoma model. Animals were subjected to DMP exposure at varying concentrations. We assessed IOP, optic nerve thickness, and expression of neurotrophic factors (NGF, BDNF). Molecular mechanisms were elucidated via Western blotting for key signaling pathways and apoptosis/inflammation markers, complemented by ELISA for oxidative stress. Functional validation was performed using specific pathway agonists and inhibitors. DMP exposure exacerbated core glaucomatous pathology in a concentration-dependent manner, significantly elevating IOP, reducing optic nerve thickness, and downregulating NGF/BDNF. Mechanistically, DMP concurrently inhibited the pro-survival PI3K/Akt pathway while activating the pro-inflammatory JAK/STAT and NF-κB pathways and the fibrotic Wnt/β-catenin pathway. This multi-pathway disruption synergistically amplified retinal oxidative stress and triggered RGC apoptosis. Rescue experiments confirmed that the modulation of these specific pathways directly influenced the observed oxidative injury and cellular damage. This study firstly demonstrated that dimethyl phosphate (DMP) does not independently induce a complete glaucomatous phenotype but significantly aggravates optic nerve damage under elevated IOP conditions. By simultaneously regulating multi-pathways and activating inflammatory and fibrotic pathways, DMP amplified oxidative stress and promoted retinal ganglion cell apoptosis. These findings supported the concept that environmental toxicants may act as disease modifiers in glaucoma progression.
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