Kessel David, Oleinick Nancy L
Department of Pharmacology, Wayne State University School of Medicine, Detroit, Michigan, USA.
Methods Enzymol. 2009;453:1-16. doi: 10.1016/S0076-6879(08)04001-9.
Photodynamic therapy (PDT) involves the irradiation of photosensitized cells with light. Depending on localization of the photosensitizing agent, the process can induce photodamage to the endoplasmic reticulum (ER), mitochondria, plasma membrane, and/or lysosomes. When ER or mitochondria are targeted, antiapoptotic proteins of the Bcl-2 family are especially sensitive to photodamage. Both apoptosis and autophagy can occur after PDT, autophagy being associated with enhanced survival at low levels of photodamage to some cells. Autophagy can become a cell-death pathway if apoptosis is inhibited or when cells attempt to recycle damaged constituents beyond their capacity for recovery. While techniques associated with characterization of autophagy are generally applicable, PDT introduces additional factors related to unknown sites of photodamage that may alter autophagic pathways. This chapter discusses issues that may arise in assessing autophagy after cellular photodamage.
光动力疗法(PDT)涉及用光照射光敏化细胞。根据光敏剂的定位,该过程可诱导对内质网(ER)、线粒体、质膜和/或溶酶体的光损伤。当内质网或线粒体成为靶点时,Bcl-2家族的抗凋亡蛋白对光损伤尤为敏感。光动力疗法后凋亡和自噬均可发生,自噬与某些细胞在低水平光损伤时存活率提高有关。如果凋亡受到抑制或细胞试图回收受损成分但超出其恢复能力,自噬可成为一种细胞死亡途径。虽然与自噬特征描述相关的技术普遍适用,但光动力疗法引入了与未知光损伤部位相关的额外因素,这些因素可能会改变自噬途径。本章讨论细胞光损伤后评估自噬时可能出现的问题。