ArticleExperimental brain research2020
The expression change of glial fibrillary acidic protein and tyrosine hydroxylase in substantia nigra of the Wistar rats exposed to chlorpyrifos: a novel environmental risk factor for Parkinson's disease.
Article in Experimental brain research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 17 citations in OpenAlex.
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- The pesticide chlorpyrifos increases the risk of Parkinson's disease.Molecular neurodegeneration · 2025Article
- Environmental Risk Factors for Parkinson's Disease: A Critical Review and Policy Implications.Movement disorders : official journal of the Movement Disorder Society · 2025Review
- The susceptibility of humans to neurodegenerative and neurodevelopmental toxicities caused by organophosphorus pesticides.Archives of toxicology · 2023Review
- Article
- Liposomal Form of L-Dopa and SH-Sy5y Cell-Derived Exosomes Modulate the Tyrosine Hydroxylase/Dopamine Receptor D2 Signaling Pathway in Parkinson's Rat Models.Journal of molecular neuroscience : MN · 2021Article
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2 authors at 2 institutions in 1 country.
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Abstract
Chlorpyrifos (CPF) is one of the most abundant and widely used pesticides in the world. CPF has detrimental effects on brain tissue, so it is possible to generate some neurodegenerative diseases. The aim of this study was to evaluate the effect of CPF on inducing the Parkinson's disease affecting on central nervous system. 6 to 8-week-old animals were categorized into three groups. The first group was normal control which the animals did not received any treatment, while in the second group, CPF were injected (CPF; 5 mg/kg BW for 30 days intraperitoneally) and the sham group as the third group received DMSO. At the end of the CPF treatment, malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured in the brain tissues of rats. Proportion of neurons was analyzed by crystal violet assays and tunnel assay to detect apoptotic cells. Finally, the expression of GFAP and TH was investigated in the brain of animals. The results witnessed an increase in MDA and a decrease in SOD (P < 0.05) after the CPF treating. Moreover, results indicated that the proportion of neurons decreased in the second group vs. normal and sham groups significantly (P < 0.001). Additionally, in substantia nigra, the expression of GFAP had a significant increase and the TH had a remarkable decrease in CPF injected group in comparison to two other groups (P < 0.001). Furthermore, the numbers of apoptosis cells reduced in substantia nigra (P < 0.001) after the 30-day period of CPF injections. These results demonstrated that repeated exposure to CPF can induce PD via apoptotic cell death, histopathological disruption. It also altered the expression of dopaminergic neuron and changes the levels of oxidant and antioxidant enzymes in substantia nigra region which triggers PD. Hence, the CPF can be introduced as a risk factor for PD.
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