Abstract
.Significance: Side effects of many cancer treatments are associated with the production of reactive oxygen species (ROS) in normal tissues. This explains why patients treated by photodynamic therapy (PDT) often suffer from skin photosensitization, whereas those subject to radiotherapies frequently experience damages in various organs, including the skin.Aim: Catechin, which belongs to the natural flavanols family, is well known for its antioxidant properties. Hence, our main objective was to investigate whether catechin can reduce damages induced by PDT using protoporphyrin IX (PpIX-PDT), an endogenous photosensitizer commonly used in dermatology.Approach: An in vivo model, the chick embryo chorioallantoic membrane (CAM), was used for this study. An amount of of a solution containing 5-aminolevulinic acid, a natural precursor of PpIX, was applied topically on the CAM 4 h before PDTs (405 nm, , ). Catechin was applied at different concentrations (1 to ) and times (0 to 240 min) before PDT. In addition, we assessed the potency of catechin to reduce the PpIX fluorescence photobleaching induced by PDT.Results: We observed that catechin significantly reduces the vascular damages generated by PpIX-PDT. Moreover, we have shown that catechin inhibits PpIX photobleaching.Conclusions: These observations suggest that catechin significantly reduces the level of ROS produced by PpIX-PDT.
Highlights
Photodynamic therapy (PDT), a minimally invasive and clinically approved procedure, is used for the treatment of different types ofcancers as well as certain forms of age-related macular degeneration.[1,2] Three key elements are involved in PDT: a nontoxic photosensitizer (PS), light that excites the PS, and molecular oxygen
We observed that catechin significantly reduces the vascular damages generated by protoporphyrin IX (PpIX)-PDT
We have shown that catechin inhibits PpIX photobleaching
Summary
Photodynamic therapy (PDT), a minimally invasive and clinically approved procedure, is used for the treatment of different types of (pre)cancers as well as certain forms of age-related macular degeneration.[1,2] Three key elements are involved in PDT: a nontoxic photosensitizer (PS), light that excites the PS, and molecular oxygen. The PS, after excitation with light, can transfer some of its energy to the latter, which leads to the production of reactive oxygen species (ROS), in particular, singlet oxygen. These ROS induce cell/tissue damages, eventually resulting in cell death by apoptosis, necrosis, and/or autophagy.[3,4,5]. One of the most extensively used PS for PDT is protoporphyrin IX (PpIX) This fluorescing PS is ubiquitously present and endogenously produced in most living cells as a penultimate step in the biosynthesis of heme.[6] Its production in certain cancer lesions can be significantly
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