Cytotoxic and prooxidant effects of an arylseleno amine (LQ20) in human neuroblastoma cells (SH-SY5Y).
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High-risk neuroblastoma is an aggressive extracranial solid tumor frequently diagnosed during early childhood. Despite advances in therapy, survival rates remain limited and treatment is often associated with severe adverse effects, highlighting the need for novel therapeutic strategies. Selenium compounds have emerged as potential anticancer agents due to their ability to disrupt cellular redox homeostasis. In the present study, we investigated for the first time the cytotoxic and pro-oxidant effects of the organoselenoamine LQ20 in human neuroblastoma SH-SY5Y cells. LQ20 reduced cell viability in a time- and concentration-dependent manner, with a CC50 of 63 µM after 72 h of treatment. Additionally, in a preliminary exploratory experiment, the cytotoxic effects of LQ20, assessed by cell viability analysis, were more pronounced in SH-SY5Y cells than in the non-tumoral neuronal cell line HT-22. In SH-SY5Y cells, the compound increased intracellular reactive oxygen species (ROS) levels by approximately twofold and reduced glutathione (GSH) levels by up to 58%, indicating alterations in cellular redox balance. LQ20 also induced mitochondrial membrane depolarization, caspase-3 activation and phosphatidylserine externalization, accompanied by morphological alterations characteristic of apoptosis. Overall, these findings indicate that LQ20 promotes apoptotic cell death in neuroblastoma cells - possibly associated with oxidative stress and mitochondrial dysfunction. These results provide new insights into the biological activity of LQ20 and support further investigation of organoselenium compounds as potential anticancer agents.