The Effect of Neuronal CoQ
Ubiquinone
/ analogs & derivatives
Rotenone
/ toxicity
Mitochondria
/ metabolism
Humans
Oxidative Stress
/ drug effects
Reactive Oxygen Species
/ metabolism
Neurons
/ metabolism
Parkinson Disease
/ metabolism
Cell Line, Tumor
Muscle Weakness
/ metabolism
Cell Survival
/ drug effects
Electron Transport Complex I
/ metabolism
Ataxia
Mitochondrial Diseases
Parkinson’s disease
antioxidant defences
coenzyme Q10
mitochondrial biogenesis
mitochondrial dysfunction
neurodegeneration
oxidative stress
pentose phosphate pathway
therapeutics
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
16 Jun 2024
16 Jun 2024
Historique:
received:
18
04
2024
revised:
12
06
2024
accepted:
14
06
2024
medline:
27
6
2024
pubmed:
27
6
2024
entrez:
27
6
2024
Statut:
epublish
Résumé
Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder currently affecting the ageing population. Although the aetiology of PD has yet to be fully elucidated, environmental factors such as exposure to the naturally occurring neurotoxin rotenone has been associated with an increased risk of developing PD. Rotenone inhibits mitochondrial respiratory chain (MRC) complex I activity as well as induces dopaminergic neuronal death. The aim of the present study was to investigate the underlying mechanisms of rotenone-induced mitochondrial dysfunction and oxidative stress in an in vitro SH-SY5Y neuronal cell model of PD and to assess the ability of pre-treatment with Coenzyme Q
Identifiants
pubmed: 38928331
pii: ijms25126622
doi: 10.3390/ijms25126622
pii:
doi:
Substances chimiques
Ubiquinone
1339-63-5
Rotenone
03L9OT429T
coenzyme Q10
EJ27X76M46
Reactive Oxygen Species
0
Electron Transport Complex I
EC 7.1.1.2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM