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  • Title: Hematoporphyrin monomethyl ether photodynamic damage on HeLa cells by means of reactive oxygen species production and cytosolic free calcium concentration elevation.
    Author: Ding X, Xu Q, Liu F, Zhou P, Gu Y, Zeng J, An J, Dai W, Li X.
    Journal: Cancer Lett; 2004 Dec 08; 216(1):43-54. PubMed ID: 15500948.
    Abstract:
    Hematoporphyrin monomethyl ether (HMME) is a novel and promising porphyrin-related photosensitizer for photodynamic therapy (PDT). HMME-PDT-induced cell death and its mechanisms were investigated in HeLa cells. We demonstrated that HMME-PDT could induce cell death through both necrosis and apoptosis. Sodium azide (the singlet oxygen quencher) or D-mannitol (the hydroxyl radical scavenger) could protect HeLa cells from the apoptosis and necrosis induced by HMME-PDT, showing that reactive oxygen species (ROS), such as singlet oxygen and hydroxyl radical, played a decisive role in HMME-PDT-induced HeLa cells death. Sodium azide or D-mannitol also inhibited HMME-PDT-mediated [Ca2+]i elevation. Cytochrome C (Cyto C) release from mitochondria into cytosol and Caspase-3 activation after HMME-PDT were inhibited by BAPTA/AM (an intracellular calcium chelator). These results demonstrated that ROS generated in HeLa cells by HMME-PDT-induced apoptosis may be through [Ca2+]i elevation which mediates Cyto C release and Caspase-3 activition and initiates the subsequent late stages of apoptosis.
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