RT Journal Article
T1 Impact of Glucocorticoid on a Cellular Model of Parkinson's Disease: Oxidative Stress and Mitochondrial Function.
A1 Claros, Silvia
A1 Gil, Antonio
A1 Martinelli, Mauro
A1 Valverde, Nadia
A1 Lara, Estrella
A1 Boraldi, Federica
A1 Pavia, Jose
A1 Martín-Montañez, Elisa
A1 Garcia-Fernandez, María
K1 Parkinson’s disease
K1 hormonal stress
K1 mitochondria
K1 oxidative distress
AB Stress seems to contribute to the neuropathology of Parkinson's disease (PD), possibly by dysregulation of the hypothalamic-pituitary-adrenal axis. Oxidative distress and mitochondrial dysfunction are key factors involved in the pathophysiology of PD and neuronal glucocorticoid-induced toxicity. Animal PD models have been generated to study the effects of hormonal stress, but no in vitro model has yet been developed. Our aim was to examine the impact of corticosterone (CORT) administration on a dopaminergic neuronal cell model of PD induced by the neurotoxin MPP+, as a new combined PD model based on the marker of endocrine response to stress, CORT, and oxidative-mitochondrial damage. We determined the impact of CORT, MPP+ and their co-incubation on reactive oxygen species production (O2-•), oxidative stress cellular markers (advanced-oxidation protein products and total antioxidant status), mitochondrial function (mitochondrial membrane potential and mitochondrial oxygen consumption rate) and neurodegeneration (Fluoro-Jade staining). Accordingly, the administration of MPP+ or CORT individually led to cell damage compared to controls (p
SN 2076-3425
YR 2021
FD 2021-08-22
LK https://hdl.handle.net/10668/28347
UL https://hdl.handle.net/10668/28347
LA en
DS RISalud
RD Apr 13, 2025