Diaz-Casado 2014 Abstract SECF

Melatonin restores mitochondrial regulatory gene expression and function in the zebrafish model of parkinsonism.

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Díaz-Casado E, Lima-Cabello E, Doerrier C, García JA, Escames G, Acuña-Castroviejo D (2014)

Event: SECF

Parkinson’s disease (PD) is a neurological disorder characterized by the progressive loss of dopaminergic (DA) neurons. Oxidative stress and inflammation are two key processes in the pathophysiology of PD. Both mechanisms are directly related to mitochondrial dysfunction and bioenergetic failure, which promotes neuronal death. The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which specifically inhibits mitochondrial complex I activity, is usually used to yied parkinsonism in roedents and zebrafish. The association between mitochondrial dysfunction and neurodegeneration is gaining experimental support in PD, which can be associated with mutations in mitochondria-associated genes including DJ-1, alpha-synuclein, Park-2 and PINK-1. Because mitochondria are the main target of melatonin actions, we evaluated here whether its neuroprotective actions depend on the regulation of these genes in the zebrafish model of PD.

To generate a zebrafish model of PD with the use of MPTP, looking for molecular targets involved in the neuroprotective effects of melatonin.

Zebrafish embryos of the AB line were used at 24 hpf. 70 zebrafish embryos were randomly divided in three groups; Control Group (C); MPTP Group (MPTP), treated with MPTP (600 μM), and aMT Group (aMT), treated with MPTP (600 μM) and aMT (1μM) during 48h. Mitochondrial respiratory function and analysis of gene expression (qRT-PCR and Western Blot) of THase, Park-7, alpha-synuclein, Park-2, Park-6, and iNOS isoform were performed.

• O2k-Network Lab: ES Granada Acuna-Castroviejo D

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