Abstract
Interaction of calf thymus DNA (CT-DNA) with two liposomes made of 1,2-dipalmitoyl-sn-glycero-3-phosphocholine (DPPC) and 1,2-dimyristoyl-sn-glycero-3-phosphocholine (DMPC) and its impact on an encapsulated anticancer drug ellipticine have been studied by steady-state and time-resolved fluorescence spectroscopy. Addition of DNA to the ellipticine impregnated liposomes causes quenching in the fluorescence intensity as DNA induces subsequent hydration and rupture of the bilayers leading to the leakage of drug molecules. We have found higher quenching in DPPC than that in DMPC liposomes at both below and above their respective phase transition temperature. Since DPPC remains less prehydrated due to its higher phase transition temperature than DMPC, therefore DNA induced hydration is higher in DPPC and this results in higher quenching. The time-resolved studies revealed that both the fast and slow lifetime components of ellipticine decrease significantly with addition of DNA due to DNA induced hydration and rupture of bilayers. Above the phase transition temperature, no such change in lifetime components takes place as bilayers already remain prehydrated and further DNA induced hydration does not occur. It is revealed that with addition of DNA to liposomes at both the temperatures, the amplitude of the fast component increases and that of slow component decreases which implies that the drug molecules are migrating to the aqueous phase, leaving the liposome hydrophobic core. The extent of migration of drug molecules is much more pronounced in DPPC compared to that in DMPC.