Study of the potential toxicity of adrenaline to neurons, using the SH-SY5Y human cellular model

Prolonged overexposure to catecholamines causes toxicity, usually credited continuous adrenoceptor stimulation, autoxidation, and the formation of reactive pro-oxidant species. Non-differentiated SH-SY5Y cells were used study possible contribution oxidative stress in adrenaline (ADR)-induced neurotoxicity, as a model predict toxicity this catecholamine peripheral nerves. Cells exposed several concentrations ADR (0.1, 0.25, 0.5 1mM) two cytotoxicity assays [lactate dehydrogenase (LDH) release 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl tetrazolium bromide (MTT) reduction] performed at time-points (24, 48, 96h). The was concentration- time-dependent both assays, since lowest concentration tested (0.1mM) also caused significant 96h. N-acetyl-cysteine (1mM), precursor glutathione synthesis, prevented ADR-induced elicited by 0.5mM 0.25mM following 96-h exposure, while antioxidant Tiron (100µM) non-protective. In conclusion, led mitochondrial distress ultimately cell death non-differentiated cells, possibly because oxidation products. involvement such processes catecholamine-induced neuropathy requires further analysis.