In addition, compound 12k was found to induce apoptosis in NCI-H460 cells via the mitochondrial pathway, including an increase of the ROS level, loss of mitochondrial membrane potential, release of cytochrome c, down-regulation of Bcl-2, up-regulation of Bax, activation of caspase-9 and caspase-3, respectively.
Disruption of the mitochondrial membrane potential, release of cytochrome c from mitochondria, up-regulation of FasL and Bax, and down-regulation of GRP78 and Bcl-2 were also observed.
Furthermore, Treatment of prostate cancer cells with resveratrol resulted in generation of reactive oxygen species (ROS), translocation of Bax to mitochondria and subsequent drop in mitochondrial membrane potential, release of mitochondrial proteins (cytochrome c, Smac/DIABLO, and AIF) to cytosol, activation of effector caspase-3 and caspase-9, and induction of apoptosis [1], [14], [15].
Furthermore, treatment of LNCaP cells with resveratrol resulted in translocation of Bax and p53 to mitochondria, production of reactive oxygen species, drop in mitochondrial membrane potential, release of mitochondrial proteins (cytochrome c, Smac/DIABLO and Omi/HtrA2), and activation of caspase-3 leading to apoptosis [41].
Mitochondrial ROS production is one of the very early events preceding collapse of mitochondrial membrane potential, release of pro-apoptotic factors, and activation of caspases [ 8].
Early loss of the mitochondrial membrane potential, release of cytochrome c and Smac (second mitochondria-derived activator of caspases) clearly indicated the activation of mitochondrial apoptosis pathways.
L.m infection or LLO stimulation decreases mitochondria membrane potential, releases its LRR suppression and induces NLRX1 oligomerization to expose its LIR motif to associate with LC3 for mitophagy induction.
It caused damage to DNA and disruption of mitochondrial membrane potential, released cytochrome c, and led to mitochondrial-dependent apoptosis [3,28,29].
Similar to our results, GS treatment has been shown to alter mitochondrial membrane potential releasing cytochrome c and initiating apoptosis leukemia, prostate and colon cancer [ 15, 16, 18].
tBid translocates to the mitochondrial membrane, where it interacts with Bax and Bak, enhancing their oligomerization and leading to outer membrane permeabilization, loss of membrane potential and release of mitochondrial apoptogens.
During apoptosis, the permeability of the mitochondrial membrane increased, leading to a loss of membrane potential and release of cytochrome c into the cytosol, which binds to apoptotic protease activating factor-1 (Apaf‑1) [ 28].
