Tumor cell response to drug induced apoptosis is a function of intra-cellular redox status

Abstract

Tumor cell response to drug induced apoptosis is efficiently regulated by a critical balance between superoxide and hydrogen peroxide. Slightly elevated levels of superoxide levels within tumor cells maintain pH in an alkaline range that bestows them a survival advantage. Contrarily, signals that induce intracellular production of hydrogen peroxide lead to cytosolic acidification that facilitates apoptosis. This thesis discusses the importance of hydrogen peroxide as being central in the apoptotic program and its potential role in Bax-mediated mitochondrial apoptosis. In my investigation, using vitamin C in photo-degradation of merocyanine-540 I have derived novel bio-active molecules that induce H2O2 mediated apoptosis. Contrarily drugs such as resveratrol can create a pro-oxidant state in tumor cells by blocking H2O2 production, eventually leading to an intracellular environment that inhibits apoptotic pathway(s). Taken together these findings will provide insight into ROS regulation and mechanisms as to how tumor cells can be tailored to undergo effective anti-cancer therapy.