Striatal mitochondria response to 3-nitropropionic acid and fish oil treatment

Autor: Francisco José Calvo-Silva, Francisca Fernández-Valverde, Marisol Orozco-Ibarra, Jazmín García-Morales, Norma Serrano-García
Rok vydání: 2016
Předmět:
Male
0301 basic medicine
Medicine (miscellaneous)
Striatum
Mitochondrion
Biology
Pharmacology
medicine.disease_cause
Antioxidants
Electron Transport Complex IV
03 medical and health sciences
chemistry.chemical_compound
Fish Oils
0302 clinical medicine
Huntington's disease
In Situ Nick-End Labeling
medicine
Animals
Rats
Wistar
Membrane potential
Nutrition and Dietetics
Dose-Response Relationship
Drug
Toxin
Electron Transport Complex II
General Neuroscience
General Medicine
Cytochrome-c Peroxidase
NAD
Nitro Compounds
Fish oil
medicine.disease
Corpus Striatum
Mitochondria
Rats
Disease Models
Animal
Oxidative Stress
Huntington Disease
Neuroprotective Agents
030104 developmental biology
chemistry
Biochemistry
Toxicity
Lipid Peroxidation
Propionates
Adenosine triphosphate
030217 neurology & neurosurgery
Zdroj: Nutritional Neuroscience. 21:132-142
ISSN: 1476-8305
1028-415X
DOI: 10.1080/1028415x.2016.1237074
Popis: Mitochondrial dysfunction is involved in neurodegenerative diseases, such as Huntington's disease (HD). 3-Nitropropionic acid (3-NP) is a mitochondrial toxin that specifically inhibits complex II of the electron transport chain (ETC) and is used to generate an experimental model of HD.To study the effect of fish liver oil (FO) over the mitochondrial dysfunction induced via partial ETC inhibition by 3-NP.This study was performed in rats and consisted of two phases: (i) administration of increasing doses of 3-NP and (ii) administration of FO for 14 days before to 3-NP. The rats' exploratory activity; complex I, II, III, and IV activities; and rearing behavior were observed. Additionally, the number of TUNEL-positive cells and various mitochondrial parameters, including oxygen consumption, transmembrane potential, adenosine triphosphate synthesis, and ETC activity, were measured.We observed that FO exerted a protective effect against the 3-NP-induced toxicity, although complex II inhibition still occurred. Instead, this effect was related to strengthened mitochondrial complex III and IV activities.Our results show that FO exerts a beneficial prophylactic effect against mitochondrial damage. Elucidating the mechanisms linking the effects of FO with its prevention of neurodegeneration could be the key to developing recommendations for FO consumption in neurological pathologies.
Databáze: OpenAIRE
Externí odkaz: