Selenomethionine activates selenoprotein S, suppresses Fas/FasL and the mitochondrial pathway, and reduces Escherichia coli-induced apoptosis of bovine mammary epithelial cells

Escherichia coli is a major environmental pathogen causing bovine mastitis, characterized by cell death and mammary tissue damage. Apoptosis, form of death, has an important role in the pathogenesis mastitis. Selenium, essential trace element, protects against mastitis acting through several biochemical pathways, potentially including prevention apoptosis. Our objective was to investigate whether selenomethionine (SeMet) attenuated E. coli-induced apoptosis epithelial cells (bMEC). These were cultured vitro treated with 0, 5, 10, 20, 40 μM SeMet for 12 h, or without (multiplicity infection 5) 8 h. Treatment SeMet/Z-IE(OMe)TD(OMe)-FMK (ZIK)/Z-LE(OMe)HD(OMe)-FMK (ZLK, specific inhibitors caspase-8 -9, respectively) significantly counteracted effects on bMEC. Specifically, upregulated selenoprotein S (SeS) increased mitochondrial membrane potential ratio Bcl-2 Bax. Furthermore, it decreased protein expressions Fas, FasL, FADD, cleaved caspase-8, cytochrome c, caspase-9, caspase-3, namely, decreasing expression Fas/FasL pathways. downregulated total indexes coli-infected Although ZIK ZLK (specific caspases 9, inhibited apoptotic pathway indexes, respectively, substantial still occurred. In conclusion, bMEC activating SeS, associated