pCramoll and rCramoll as New Preventive Agents against the Oxidative Dysfunction Induced by Hydrogen Peroxide

Figure 8

Schematic overview of the protective effects of pCramoll and rCramoll on the H₂O₂-induced cell death. (a) H₂O₂ can induce cell dysfunction due its capacity to interact directly or indirectly with organelles and cell membrane causing lipid peroxidation, leakage of lysosomal content, DNA damage, decrease in the mitochondrial membrane potential, and increase of mitochondrial ROS production, thereby disrupting cellular function and integrity. (b) The binding of both pCramoll and rCramoll to specific glycosylated targets on the surface of Vero cells or intracellularly can trigger the antioxidant mechanisms of cells that prevent the deleterious effects of H₂O₂ on organelles such as mitochondria, lysosomes, and nucleus, promoting cell survival and proliferation. (c and d) Alternatively, both lectins can act directly as H₂O₂ or/and secondary ROS scavengers, neutralizing the harmful effects of oxidative stress.

(a)

(b)

(c)

(d)