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
in En
| LILACS
| ID: biblio-1439510
Responsible library:
BR40.1
Localization: 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.
Key words
Full text:
1
Index:
LILACS
Main subject:
Epinephrine
/
Peripheral Nervous System Diseases
/
Toxicity
/
Neurons
Type of study:
Prognostic_studies
Language:
En
Journal:
Braz. J. Pharm. Sci. (Online)
Journal subject:
Farmacologia
/
Teraputica
/
Toxicologia
Year:
2023
Type:
Article