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.
CPF
GFAP
Parkinson’s disease
Substantia nigra
TH
Journal
Experimental brain research
ISSN: 1432-1106
Titre abrégé: Exp Brain Res
Pays: Germany
ID NLM: 0043312
Informations de publication
Date de publication:
Sep 2020
Sep 2020
Historique:
received:
16
05
2020
accepted:
01
07
2020
pubmed:
8
7
2020
medline:
29
7
2021
entrez:
8
7
2020
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 32632573
doi: 10.1007/s00221-020-05868-x
pii: 10.1007/s00221-020-05868-x
doi:
Substances chimiques
Glial Fibrillary Acidic Protein
0
Tyrosine 3-Monooxygenase
EC 1.14.16.2
Chlorpyrifos
JCS58I644W
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM