Figure 9. Proposed model for mechanism of 4a induced cytotoxicity by induction of apoptosis.

4a treatment resulted in production of ROS, thereby damaging the DNA, which in turn helped in upregulation and phosphorylation of p53, where it activated extrinsic pathway of apoptosis by activating FAS, cleavage of FAS-L. These activated death receptors resulted in the recruitment of adaptor proteins, FAS-associated death domain proteins (FADD), which recruits and aggregates CASPASE-8, thereby promoting its auto processing and activation. Activated CASPASE-8 cleaves BID into t-BID, which further facilitates in the release of CYTOCHROME C from mitochondria, further cleaving PROCASPASE-3 into the effector CASPASE-3 which leads to cell death.