GSE135381
Dietary selenium-methionine affects the levels and toxicity of methylmercury in Balb-C mice
Methylmercury (MeHg) is a well-known neurotoxicant, particularly harmful for the developing brain. Selenium is a nutrient previously shown to interact with MeHg, however the molecular mechanisms behind these interaction is not fully described. To explore the effect of selenium on MeHg, mice were exposed to selenomethionine (SeMet) and MeHg in a 2 x 3 full factorial design for 12 weeks. After termination, organs, including the brain, were collected for Hg and Se analysis. The hippocampus was collected and analysed using gel free proteomics and RNA sequencing (RNA-seq).  The presence of SeMet reduced the amount of Hg in several organs, including the brain, while the level of Hg were increased in the feces. The presence of Hg also increased the concentration of selenium in liver and cortex. Proteomic and RNA-seq analyses showed that several known pathways of MeHg toxicity, such as oxidative stress, altered metabolism and calcium disruption were alleviated when SeMet were present. Our results suggest that SeMet can to a certain extent ameliorate the neurotoxic effects of MeHg in a mouse model. Although, whether this is due to decrease of body burden of Hg or through direct interactions with selenium in vivo remains unclear. Overall design: Mice were orally exposed to selenium and two different doses of mercury in a full factorial design. Exposure groups; no selenium and no mercury (Ctr), selenium (Se_Ctr), high dose mercury (HD), low dose mercury (LD), selenium and high dose mercury (Se_HD), selenium and low dose mercury (Se_LD).