TRPM2 channel contribution to CdCI2-related neurotoxicity in SH-SY5Y cells: Protective role of selenium

Humans are most exposed to the heavy metal cadmium (Cd), known as neurotoxic. However, it is unclear how selenium (Se) protects neurons from damage caused by increased Cd-induced neurotoxicity in SH-SY5Y cells and how the TRPM2 channel functions in this process. In this study, we examined the impact of Se on CdCI₂-induced oxidative neurotoxicity and cell death in SH-SY5Y cells by modifying the TRPM2 channel. The Se and TRPM2 channel antagonist 2-APB was added to prevent CdCI₂-induced neurotoxicity in SH-SY5Y cells. Cell viability rate was determined between groups by CCK-8 assay. GSH, MDA, and ROS levels were determined in the cells with ELISA kits. Our results showed that the TRPM2 channel plays a vital role in forming CdCI₂-induced damage to cells by using the TRPM2 antagonist in the study. We also observed that Se reduced CdCI₂-induced neurotoxicity by reducing TRPM2 channel activation by suppressing oxidative stress of cells. We conclude that Se therapy and TRPM2 channel blocking can reduce CdCI₂-induced neurotoxicity based on our investigation, which examined the protective impact of Se and the involvement of the TRPM2 channel in CdCI₂-induced SH-SY5Y cells for the first time.

 Keywords: Cadmium, Selenium, SH-SY5Y cells, TRPM2 channel