Neurotoxicology 26(4):721–728Ĭaughlan A, Newhouse K, Namgung U, Xia Z (2004) Chlorpyrifos induces apoptosis in rat cortical neurons that is regulated by a balance between p38 and ERK/JNK MAP kinases. Neurotoxicology 43:82–89Ĭaudle WM, Richardson JR, Wang M, Miller GW (2005) Perinatal heptachlor exposure increases expression of presynaptic dopaminergic markers in mouse striatum. Mol Brain 3(1):1–20Ĭarr RL, Graves CA, Mangum LC, Nail CA, Ross MK (2014) Low level chlorpyrifos exposure increases anandamide accumulation in juvenile rat brain in the absence of brain cholinesterase inhibition. J Nepal Health Res Councilīinukumar B, Bal A, Kandimalla RJ, Gill KD (2010) Nigrostriatal neuronal death following chronic dichlorvos exposure: crosstalk between mitochondrial impairments, α synuclein aggregation, oxidative damage and behavioral changes. Lancet Neurol 15(12):1257–1272īajracharya SR, Prasad PN, Ghimire R (2017) Management of organophosphorus poisoning. J Neurosci Methods 159(2):195–202Īscherio A, Schwarzschild MA (2016) The epidemiology of Parkinson’s disease: risk factors and prevention. Neurotox Res 36(4):700–711Īllbutt HN, Henderson JM (2007) Use of the narrow beam test in the rat, 6-hydroxydopamine model of Parkinson’s disease. Hence, the CPF can be introduced as a risk factor for PD.Īli SJ, Ellur G, Patel K, Sharan K (2019) Chlorpyrifos exposure induces parkinsonian symptoms and associated bone loss in adult Swiss Albino Mice. It also altered the expression of dopaminergic neuron and changes the levels of oxidant and antioxidant enzymes in substantia nigra region which triggers PD. These results demonstrated that repeated exposure to CPF can induce PD via apoptotic cell death, histopathological disruption. Furthermore, the numbers of apoptosis cells reduced in substantia nigra ( P < 0.001) after the 30-day period of CPF injections. 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). normal and sham groups significantly ( P < 0.001). Moreover, results indicated that the proportion of neurons decreased in the second group vs. The results witnessed an increase in MDA and a decrease in SOD ( P < 0.05) after the CPF treating. Finally, the expression of GFAP and TH was investigated in the brain of animals. Proportion of neurons was analyzed by crystal violet assays and tunnel assay to detect apoptotic cells. At the end of the CPF treatment, malondialdehyde (MDA) and superoxide dismutase (SOD) levels were measured in the brain tissues of rats. 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. 6 to 8-week-old animals were categorized into three groups. The aim of this study was to evaluate the effect of CPF on inducing the Parkinson’s disease affecting on central nervous system. CPF has detrimental effects on brain tissue, so it is possible to generate some neurodegenerative diseases. Chlorpyrifos (CPF) is one of the most abundant and widely used pesticides in the world.
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