Fig. 2.
Schematic representation of mitochondrial function explains the reason for target mitochondria. (a) Dequalinium binds to the mitochondrial DNA (mtDNA) and blocks the DNA synthesis. (b) RLA peptide (D[RLARLAR]2) targets the mitochondrial outer membrane by increasing the membrane permeability and drug accumulation. (c) Gramicidin S acts as an electron scavenger and damages the mitochondrial membrane. (d) Paclitaxel/Nocadozole/Vinonelbine increases the release of cytochrome C and induces apoptosis. (e) Arsenic trioxide which binds to the voltage dependent anionic channel (VDAC) that alters the function of VDAC and mitochondria permeability transition pore complex (mPTPC). It also inhibits blocks the respiratory enzymes resulting in induction of apoptosis. (f) Gamitrinibs inhibit and target the activity of heat shock protein 90 (HSP90) in the mitochondria of human cancer cells by acting as ATPase antagonists and modulating tumor necrosis factor receptor-associated protein 1 (TRAP1) and, exerts apoptotic functions. Thus, drugs specifically targeted to mitochondria display tumor-selective cytotoxic properties results in induction of tumor cell death.