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Fig. 6 | BMC Pharmacology and Toxicology

Fig. 6

From: Heme oxygenase-1 attenuates cadmium-induced mitochondrial-caspase 3- dependent apoptosis in human hepatoma cell line

Fig. 6

Proposed mechanisms for HO-1 intervention in Cd-induced apoptosis and necrosis in HepG2 cells. CdCl2 dissociates in the cells to produce Cd ion (Cd2+) (a), which can induce mitochondrial permeability transition pore by modifying the thiol groups of the membrane proteins (b), resulting in the leakage of electrons to generate ROS (c). ROS can activate Bax (d) and resulting in its migration into the mitochondrial membrane (e) with the consequent release of cytochrome c into the cytosol (f). The cytochrome c caused the activation of caspase 3 to initiate apoptosis (g). ROS generated could also activate calpain (h) which can further activate caspase 3 (i). Cd2+ can also directly activate calpain by mimicking Ca2+ ion (j). The activation of caspase 3 and calpain can result in apoptosis (k) and necrosis (l) respectively. HO-1 can attenuate ROS produced either by direct effects of Cd2+ on cellular molecules (m) or by indirect effects of Cd2+ on mitochondrial membrane permeability (c), resulting in calpain inhibition and blockage of Bax mobilization to the mitochondrial membrane

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