The pro-inflammatory oxidant hypochlorous acid induces Bax-dependent mitochondrial permeabilisation and cell death through AIF-/EndoG-dependent pathways

FPOA induces the apoptosis of HepG2 cells

“…The present study revealed that FPOA downregulated the expression of the Bcl-2 protein and upregulated the expression of Bax protein in HepG2 cells, resulting in a significant increase in the Bax/Bcl-2 ratio and inducing apoptosis. An increased Bax/Bcl-2 ratio increases mitochondrial membrane permeability, allowing cytochrome c to combine with other factors and activate caspase family proteins, triggering apoptosis (27). The present study also identified an increase in cytochrome c release from the mitochondria as the Bax/Bcl-2 ratio increased.…”

Embryonic exposure to cypermethrin induces apoptosis and immunotoxicity in zebrafish (Danio rerio)

“…In addition, Puma (a p53-dependent proapoptotic Bcl2 member) mRNA expression was also significantly up-regulated in 3 and 10 mg/l CYP-treated groups, suggesting that this gene is activated in apoptotic cell death [19]. Moreover, during apoptotic stimulation, alteration of the Bcl2/Bax protein ratio would affect mitochondrial cytochrome c release [32], and the decrease in the Bcl2/Bax ratio is considered a decisive correlation in apoptosis or cell death [33]. In the cytosol, cytochrome c interacts with Apaf1 leading directly to the activation of Cas9 [7].…”

Antitumor effect and underlying mechanism of RGD-modified adenovirus mediated IL-24 expression on myeloid leukemia cells

“…The increase of the Bax/Bcl-2 ratio alters mitochondrial membrane permeability, resulting in the release of cytochrome C in the mitochondrion. Cytochrome C combines with other factors, activating the Caspase family [30]. Activation of the family of Caspases is known as a crucial mechanism for the induction of death signals to apoptosis.…”