Figure 6
From: The Involvement of Bax in Zinc-Induced Mitochondrial Apoptogenesis in Malignant Prostate Cells
A representation of the integrated apoptogenic effects of zinc. Zinc increases the Bax-associated mitochondrial pore forming process that results in the release of cytochrome c that initiates the caspase cascade leading to apoptosis. Zinc also increases the gene expression and cellular production of Bax and the Bax/Bcl-2 ratio, which facilitates the mitochondrial Bax-associated apoptogenic effect.