Selenite protects human peripheral blood mononuclear cells (PBMCs) from CdCl2 cytotoxicity.

The potential role of selenium (Se) in modulating cadmium (Cd) cytotoxicity in human peripheral blood mononuclear cells (PBMCs) was investigated by assessing pro- and anti-inflammatory as well as redox biomarkers. We also examined the potential synergistic effects of SARS-CoV-2 N-protein with Cd in PBMCs. PBMCs were isolated from adults and treated for 48 h with sodium selenite (Na₂SeO₃; 0.04, 0.4, and 4 µM) and cadmium chloride (CdCl₂; 0.1 and 1 µM), in the presence or absence of SARS-CoV-2 N-protein. We measured total Se and Cd levels, cell viability, cytotoxicity, intracellular reactive oxygen species (ROS) production, and gene expression. Na₂SeO₃ antagonized CdCl₂-induced toxicity in PBMCs. This protective effect was associated with increased expression of antioxidant selenoprotein mRNAs, including GPX1, GPX4, TXNRD1, SELENOP, SELENOS, and SELENOK. Notably, even low concentrations of Na₂SeO₃ effectively protected PBMCs from Cd-induced toxicity, reversing cell death and restoring MTT reduction. Cd exposure slightly increased DCFH oxidation, which was abolished by Na₂SeO₃. While Cd did not markedly elevate ROS, it consistently increased inflammatory markers. Importantly, Na₂SeO₃ upregulated anti-inflammatory mRNAs (IL-4, IL-10), even in the presence of CdCl₂. These findings suggest that, regardless of SARS-CoV-2 N-protein presence, sufficient Se levels-and consequently, proper selenoprotein expression-are crucial for modulating inflammation, preventing ROS overproduction, and mitigating oxidative stress in human PBMCs.