Figure 5.

Modulation of the gut microbiota dependent on Se status and biotransformation of Se derivatives. Given the adequate intake of Se, homeostasis occurs due to the beneficial relationship between intestinal and host bacteria resulting in the biotransformation of Se compounds (Se salts metabolized into SeMet and SeCys). Se deficiency results in increased Se uptake by bacteria (Escherichia coli, Clostridia, and Enterobacteria), biotransformation of Se compounds (Se salts metabolized into SeMet and SeCys), decreased expression of selenoproteins by the host, decreased activation of Se immune cells, increased pro-inflammatory cytokines, and increased risk for IBD and cancer. On the other hand, excessive intake of Se causes increased uptake by bacteria such as Turicibacter, Akkermansi, and Lactic acid bacteria (LAB), biotransformation of Se compounds such as selenite (Se${\text{O}}_3^{2-}$) and selenate (Se${\text{O}}_4^{2-}$) which are metabolized into SeMet and SeCys, and increased excretion of volatile compounds from Se. Se, selenium; SeMet, selenomethionine; SeCys, selenocysteine; IBD, inflammatory bowel diseases (Figure illustration by Francisco Irochima Pinheiro).