Study of the potential toxicity of adrenaline to neurons, using the SH-SY5Y human cellular model
Braz. J. Pharm. Sci. (Online)
; 59: e20467, 2023. graf
Article
en En
| LILACS
| ID: biblio-1439510
Biblioteca responsable:
BR40.1
Ubicación: BR40.1
ABSTRACT
Abstract Prolonged overexposure to catecholamines causes toxicity, usually credited to continuous adrenoceptor stimulation, autoxidation, and the formation of reactive pro-oxidant species. Non-differentiated SH-SY5Y cells were used to study the possible contribution of oxidative stress in adrenaline (ADR)-induced neurotoxicity, as a model to predict the toxicity of this catecholamine to peripheral nerves. Cells were exposed to several concentrations of ADR (0.1, 0.25, 0.5 and 1mM) and two cytotoxicity assays [lactate dehydrogenase (LDH) release and 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl tetrazolium bromide (MTT) reduction] were performed at several time-points (24, 48, and 96h). The cytotoxicity of ADR was concentration- and time-dependent in both assays, since the lowest concentration tested (0.1mM) also caused significant cytotoxicity at 96h. N-acetyl-cysteine (1mM), a precursor of glutathione synthesis, prevented ADR-induced toxicity elicited by 0.5mM and 0.25mM ADR following a 96-h exposure, while the antioxidant Tiron (100µM) was non-protective. In conclusion, ADR led to mitochondrial distress and ultimately cell death in non-differentiated SH-SY5Y cells, possibly because of ADR oxidation products. The involvement of such processes in the catecholamine-induced peripheral neuropathy requires further analysis.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
LILACS
Asunto principal:
Epinefrina
/
Enfermedades del Sistema Nervioso Periférico
/
Toxicidad
/
Neuronas
Tipo de estudio:
Prognostic_studies
Idioma:
En
Revista:
Braz. J. Pharm. Sci. (Online)
Asunto de la revista:
Farmacologia
/
Teraputica
/
Toxicologia
Año:
2023
Tipo del documento:
Article
País de afiliación:
Portugal
/
Estados Unidos