Abstract
Photosensitizers (PSs) used in photodynamic therapy (PDT) have been developed to selectively destroy tumor cells. However, PSs recurrently reside on the extracellular matrix or affect normal cells in the vicinity, causing side effects. Additionally, the membrane stability of tumor cells and normal cells in the presence of reactive oxygen species (ROS) has not been studied, and the effects of ROS at the membrane level are unclear. In this work, we elucidate the stabilities of model membranes mimicking tumor cells and normal cells in the presence of ROS. The model membranes are constructed according to the degree of saturation in lipids and the bilayers are prepared either in symmetric or asymmetric form. Interestingly, membranes mimicking normal cells are the most vulnerable to ROS, while membranes mimicking tumor cells remain relatively stable. The instability of normal cell membranes may be one cause of the side effects of PDT. Moreover, we also show that ROS levels are controlled by antioxidants, helping to maintain an appropriate amount of ROS when PDT is applied.
Highlights
Various methods have been developed for cancer therapy, one of which is photodynamic therapy (PDT), where photosensitizers (PSs) accumulate in cancer cells and generate reactive oxygen species (ROS) upon light radiation [1]
Our results indicate that the side effects of PDT can be attributed to the membrane stability of normal cells and may be problematic, since the membrane composition of normal cells is more susceptible to ROS
We made model membranes mimicking normal cells and cancer cells to elucidate membrane stability in the presence of ROS and to determine how ROS levels could be controlled by antioxidants
Summary
Various methods have been developed for cancer therapy, one of which is photodynamic therapy (PDT), where photosensitizers (PSs) accumulate in cancer cells and generate reactive oxygen species (ROS) upon light radiation [1]. ROS damage intracellular components such as DNA, proteins, and lipids, inhibiting cancer cell activity [2,3]. They oxidize intracellular signaling molecules, leading to various pathways of cell death. Cell death is induced by breaking the equilibrium by the addition of ROS. These photodynamic treatments causing the apoptotic and necrotic cell death of cancer cells [6,7] have been continuously proposed since skin cancer treatment was first introduced in 1978 [8]
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