Selenium influence on gene expression in mouse brain and liver tissue

Abstract

Selenium is an essential microelement involved in antioxidant defence, redox regulation, and cellular signalling. Both its inorganic form, sodium selenite (Na₂SeO₃), and organic form, selenomethionine (SeMet), influence gene expression related to oxidative stress, apoptosis, and cell survival. The brain and liver, being highly vulnerable to oxidative stress, are critical tissues in understanding selenium’s biological effects. This study evaluates the impact of sodium selenite and selenomethionine on gene expression in these tissues, focusing on genes involved in redox regulation (MsrB1), apoptosis (Caspase-3), and cell cycle control (GADD45). The study was performed on 4-6-week-old BALB/c mice, which were divided into 4 experimental groups, that were given solutions of different concentrations of SeMet or Na₂SeO₃ (0.2 and 0.4 mg Se/kg body weight) for 8 weeks, and a control group that had free access to tap water. Then, mRNA was extracted from mouse liver and brain tissues and used to synthesize cDNA for RT-PCR analysis. The results show that MsrB1 expression in both brain and liver was higher in mice receiving 0.2 mg Se/kg of either SeMet or Na₂SeO₃ compared to the control group and those receiving 0.4 mg Se/kg. Caspase-3 expression in brain and liver was increased in mice receiving 0.2 mg Se/kg of Na₂SeO₃, but lower in those receiving 0.2 mg Se/kg of SeMet compared to the control group and those given 0.4 mg Se/kg of either selenium form. GADD45 expression in the brain and liver was elevated in mice given 0.2 mg Se/kg of Na₂SeO₃, while in SeMet-treated mice, GADD45 expression in the liver increased with higher concentrations, whereas in the brain, it decreased with increasing SeMet dosage. Overall, Na₂SeO₃ may promote stronger oxidative stress defence and apoptosis regulation, while SeMet could be more selective in its influence on apoptosis and cell cycle control, depending on tissue type.