Proceedings of the Food and Drug Administration public workshop on pathogen reduction technologies for blood safety 2018 (Commentary, p. 3026)

Atreya, Chintamani; Glynn, Simone; Busch, Michael; Kleinman, Steve; Snyder, Edward; Rutter, Sara; AuBuchon, James; Flegel, Willy; Reeve, David; Devine, Dana; Cohn, Claudia; Custer, Brian; Goodrich, Raymond; Benjamin, Richard J.; Razatos, Anna; Cancelas, Jose; Wagner, Stephen; Maclean, Michelle; Gelderman, Monique; Cap, Andrew; Ness, Paul

Speaker's summary: Photochemicals localize at nucleic acid target sites as well as off-target locations in the supernatant or bound to RBCs or PLTs. Upon illumination, photochemicals bound to target produce singlet oxygen or other ROS or are involved with electron transfer and adduct formation, preventing further replication of the pathogen. Photochemicals localized in the supernatant can produce ROS, which can diffuse to the PLT or RBC membrane to produce oxidative damage or undergo electron transfer with other colocalized photochemicals, producing photochemical dimers. Photochemicals bound to the RBC or PLT membrane produce ROS, which can oxidize membrane components or produce covalent adducts to polyunsaturated lipids via electron transfer. 170 Off-target lesions are responsible for alterations of in vitro or in vivo properties of photochemically treated RBCs and PLTs. Most photochemicals are composed of fused rings of conjugated double bonds. When a photochemical absorbs light, it cannot dissipate the absorbed energy via bond rotation as heat because of the rigidity of the ring structure and therefore releases energy via fluorescence, phosphorescence, or photochemical reactions. On the other hand, flexible photosensitizers can dissipate absorbed light energy through bond rotation and, therefore, cannot readily act as a photochemical unless rigidly bound to substrate in a planar geometry.