Fig. 2.

Schematic representation of possible Se effects against Cd-induced intoxication observed in recent animal and cell culture models. The three following basic Se effects (1) inhibition of Cd accumulation via formation of Cd–Se complexes, (2) stimulation of GPx and TrxR activity, and (3) activation of the Nrf2 factor most probably contribute to (4) a decrease in Cd-induced oxidative stress generation followed by (5) stabilization of mitochondria and ER and blockade of Cd-induced apoptosis and (6) decreased synthesis of inflammatory mediators, which in turn reduces Cd-mediated inflammation. ↑, increased; ↓, decreased