Gabriel OG, Pacheco MFP, Macías-Islas MÁ, Jiménez-Gil FJ, Miranda-Díaz AG, Flores-Alvarad LJ, Cruz-Rámos JA, Mórales-Sánchez EW, Ramírez-Ramírez V, Alatorre-Jiménez M, Bitzer-Quintero OK

Language: Spanish
References: 27
Page: 33-39
PDF size: 134.04 Kb.

ABSTRACT

Epidemiological data in humans and studies in animal models of Parkinson’s disease (PD) suggest that sporadic forms of the disorder are not strictly genetic in nature but most likely because of combined environmental exposures over the period of the life-span coupled with increased genetic susceptibilities. Exposure to agricultural chemicals such as paraquat, diquat, maneb, rotenone, and dieldrin has been separately suggested as potential risk factors for sporadic forms of the disease. In addition, exposure to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a by-product of synthetic heroine causes a clinical condition almost identical to PD. Interestingly, paraquat and MPTP share striking structural similarities. There is a growing consensus that oxidative stress and inflammation plays a key role in PD. Using a rodent model we found that melatonin attenuates the increases in lipid peroxidation products, nitric oxide catabolites and ciclooxygenase 2 activity elicited by MPTP injection. These data suggest that neuroprotective effects of melatonine are partly attributed to its antioxidant and anti-inflammatory action.

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