Figure 2.

Molecular mechanisms of RV in reducing Cd toxicity at the cellular level. Cd can disrupt the oxidative/antioxidative status of cells, indirectly resulting in oxidative stress via weakening the antioxidative barrier by inducing ROS formation and increasing electron leakage from the mitochondrial respiratory chain, ultimately leading to mitophagy. The highly stressed cell state is also reflected in the ER, where inflammasome formation and activation occur due to the altered metabolic/enzymatic environment, eventually leading to pyroptosis. RV antioxidant action can revert stressful circumstances in both organelles by reducing ROS generation and counterbalancing the inflamed environment by activating antioxidant pathways and enhancing genes relevant to the cellular stress response via epigenetic modifications. At the molecular level, Cd action also activates various pathways, initiating defense responses and leading to apoptosis by over-activating EGFR and acting on multiple points of its signaling cascades. RV beneficial effects on the cell rely on activating specific effectors that exert their inhibitory potential directly on the most critical components of signaling cascades, effectively restoring phenotype by lowering the detrimental effects of their aberrant activation.