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In Vivo Determination of Mitochondrial Respiration in 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Treated Zebrafish Reveals the Efficacy of Melatonin in Restoring Mitochondrial Normalcy.

Authors
  • Díaz-Casado, María E1, 2
  • Rusanova, Iryna1, 2
  • Aranda, Paula1, 2
  • Fernández-Ortiz, Marisol1, 2
  • Sayed, Ramy K A1, 3
  • Fernández-Gil, Beatriz I1, 2
  • Hidalgo-Gutiérrez, Agustín1, 2
  • Escames, Germaine1, 2
  • López, Luis C1, 2
  • Acuña-Castroviejo, Darío1, 2, 4
  • 1 1 Instituto de Biotecnología, Centro de Investigación Biomédica, Parque Tecnológico de Ciencias de la Salud, Universidad de Granada , Granada, Spain . , (Spain)
  • 2 2 Departamento de Fisiología, Facultad de Medicina, Universidad de Granada , Granada, Spain . , (Spain)
  • 3 3 Department of Anatomy and Embryology, Faculty of Veterinary Medicine, Sohag University , Sohag, Egypt . , (Egypt)
  • 4 4 Unidad de Gestión Clínica de Laboratorios Clínicos, CIBER de Fragilidad y Envejecimiento, Ibs.Granada, Complejo Hospitalario de Granada , Granada, Spain . , (Spain)
Type
Published Article
Journal
Zebrafish
Publication Date
Feb 01, 2018
Volume
15
Issue
1
Pages
15–26
Identifiers
DOI: 10.1089/zeb.2017.1479
PMID: 29185873
Source
Medline
Keywords
License
Unknown

Abstract

Although mitochondria dysfunction is related to multiple diseases, no in vivo studies are available on mitochondrial respiration in animal parkinsonian models. Our aim is to analyze in vivo mitochondrial respiration, which reflects changes in mitochondrial bioenergetics more precisely than in vitro mitochondrial preparations. These experiments can be carried out in zebrafish embryos, which were treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) from 24 to 72 hours postfertilization (hpf). A reduction in electron transfer system capacity, ATP turnover, and increased proton leak were observed at 72 hpf in MPTP-treated embryos. These changes were followed by a significant oxidative stress due to inhibition in antioxidative defense and autophagy impairment. After removing MPTP from the treatment at 72 hpf, these bioenergetic deficiencies persisted up to 120 hpf. The administration of melatonin to zebrafish embryos at 72 hpf, when mitochondrial dysfunction is already present, restored the respiratory capacity and ATP production, reduced oxidative stress, and normalized autophagy after 48 h. Melatonin also counteracted mortality and embryonic malformations due to MPTP. Our results confirm for the first time the efficacy of melatonin in restoring parkinsonian phenotypes in animals.

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