Hematoporphyrin monomethyl ether photodynamic damage on HeLa cells by means of reactive oxygen species production and cytosolic free calcium concentration elevation

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...

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Bibliographic Details
Published in:Cancer letters 2004-12, Vol.216 (1), p.43-54
Main Authors: Ding, Xinmin, Xu, Qinzhi, Liu, Fanguang, Zhou, Pingkun, Gu, Ying, Zeng, Jing, An, Jing, Dai, Weide, Li, Xiaosong
Format: Article
Language:English
Subjects:
Apoptosis
Binding sites
Calcium - metabolism
Calcium - pharmacokinetics
Cell Death
Clinical trials
Cytosolic free calcium concentration
Endoplasmic reticulum
Female
HeLa Cells
Hematoporphyrin monomethyl ether
Hematoporphyrins - pharmacology
Humans
Light
Necrosis
Oxygen
Photochemotherapy
Photodynamic therapy
Reactive Oxygen Species
Studies
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Summary: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 [Ca 2+] 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 [Ca 2+] i elevation which mediates Cyto C release and Caspase-3 activition and initiates the subsequent late stages of apoptosis.
ISSN:0304-3835
1872-7980
DOI:10.1016/j.canlet.2004.07.005