Photochemotherapy of Cancer: Experimental Research

Moan, Johan Emelian; Berg, Kristian

doi:10.1111/j.1751-1097.1992.tb08541.x

Cited by 369 publications

(170 citation statements)

References 220 publications

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“…Photodynamic therapy (PDT) is a novel treatment for cancer and other abnormal tissues that employs a photosensitiser and visible light to produce singlet oxygen and other reactive oxygen species (Weishaupt et al, 1976;Moan and Berg, 1992) (Peng et al, 1996). PDT is an efficient inducer of apoptosis, with the initiating reactions dependent upon the preferential sites of photosensitiser localisation.…”

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confidence: 99%

Bax is essential for mitochondrion-mediated apoptosis but not for cell death caused by photodynamic therapy

et al. 2003

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The role of Bax in the release of cytochrome c from mitochondria and the induction of apoptosis has been demonstrated in many systems. Using immunocytochemical staining, we observed that photodynamic therapy (PDT) with the photosensitiser Pc 4 induced Bax translocation from the cytosol to mitochondria, and the release of cytochrome c from mitochondria as early signalling for the intrinsic pathway of apoptosis in human breast cancer MCF-7c3 cells. To test the role of Bax in apoptosis, MCF-7c3 cells were treated with Bax antisense oligonucleotides, which resulted in as much as a 50% inhibition of PDT-induced apoptosis. In the second approach, Bax-negative human prostate cancer DU-145 cells were studied. Following PDT, the hallmarks of apoptosis, including the release of cytochrome c from mitochondria, loss of mitochondrial membrane potential, caspase activation, and chromatin condensation and fragmentation, were completely blocked in these cells. Restoration of Bax expression in DU-145 cells restored apoptosis, indicating that the resistance of DU-145 cells to PDT-induced apoptosis is due to the lack of Bax rather than to another defect in the apoptotic machinery. However, despite the inhibition of apoptosis, the Bax-negative DU-145 cells were as photosensitive as Bax-replete MCF7c3 cells, as determined by clonogenic assay. Thus, for Pc 4-PDT, the commitment to cell death occurs prior to Bax activation.

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confidence: 99%

Bax is essential for mitochondrion-mediated apoptosis but not for cell death caused by photodynamic therapy

et al. 2003

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“…PDT is a treatment for cancer and other abnormal tissue that employs a photosensitizer and visible light to produce singlet oxygen and other reactive oxygen species (Weishaupt et al, 1976), which cause an oxidative stress in cells and membrane damage (Moan and Berg, 1992) and eventually leads to cell death and tumour ablation (reviewed in Dougherty, 1993;Dougherty et al, 1998). PDT with photosensitizers that localize in the mitochondria induces rapid apoptosis (Agarwal et al, 1991;Dougherty, 1993;He et al, 1994;Luo et al, 1996;Luo and Kessel, 1997;Dougherty et al, 1998;Oleinick and Evans, 1998), probably because the photochemical damage directly targets mitochondria (Kessel and Luo, 1998) to elicit the rapid release of cytochrome c that initiates caspase-9 activation, subsequent steps in the caspase cascade, and morphological apoptosis (Kroemer et al, 1997;Granville et al, 1998Granville et al, , 1999Kessel and Luo, 1999;Varnes et al, 1999).…”

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confidence: 99%

Dissociation of mitochondrial depolarization from cytochrome c release during apoptosis induced by photodynamic therapy

2001

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Photodynamic therapy (PDT) with the phthalocyanine photosensitizer Pc 4 induces rapid apoptosis in mouse lymphoma (LY-R) cells, initiating with the release of cytochrome c from mitochondria. It has been proposed that the opening of the mitochondrial membrane permeability transition pores, which results in the dissipation of the mitochondrial membrane potential (Δψ m ), is essential for the escape of cytochrome c from mitochondria into the cytosol as well as for apoptotic cell death. Therefore, we have assessed the correlation between the loss of Δψ m and the release of cytochrome c following PDT. Treatment of LY-R cells with 300 nM Pc 4 and 60, 90 or 120 mJ/cm 2 of red light resulted in apoptosis of 80–90% of the cells, accompanied by >20-fold elevation in caspase-3-like activity within one h. At all 3 doses of PDT employed here, the majority of the cytochrome c was released from mitochondria at 15 min after irradiation, as determined by an immunohistochemical method. In contrast, the loss of Δψ m following PDT, as monitored by the uptake of JC-1 or Rh-123, depended on the PDT dose and the post-treatment time. In spite of the release of cytochrome c at 15 min after each of the 3 doses, a corresponding loss of Δψ m was observed only for those cells that received the highest dose of PDT. Virtually all cells that received one of the lower doses of PDT (300 nM Pc 4 plus 60 or 90 mJ/cm 2 ) maintained normal Δψ m . Hence, our results support the conclusion that the release of cytochrome c from mitochondria resulting from Pc 4-PDT-induced photodamage is independent of the loss of Δψ m . Therefore, it is important to consider a range of doses of this or other apoptotic stimuli in deciphering the relationship of metabolic responses that contribute to apoptosis. © 2001 Cancer Research Campaign http://www.bjcancer.com

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“…Cytotoxicity in itro resulting from porphyrin photosensitization has been well documented and a number of subcellular sites have been implicated as sites of damage, including plasma membrane, nucleus, mitochondria and lysosomes (reviewed in [15,25,26]). Many observations from published results suggest that, in the cytoplasm, mitochondria are the major target of photodynamic attack.…”

Section: Discussionmentioning

confidence: 99%

“…These sensitizers are currently used in the photodynamic therapy of solid tumours [15,16]. Photodynamic therapy causes repairable injury as well as irreversible damage leading to cell death (apoptosis and necrosis).…”

Section: Introductionmentioning

confidence: 99%

Photodynamic action of porphyrin on Ca2+ influx in endoplasmic reticulum: a comparison with mitochondria

Ricchelli

Barbato

Milani

et al. 1999

Biochemical Journal

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We have studied the distribution properties of haematoporphyrin (HP) and protoporphyrin (PP) in mitochondria and endoplasmic reticulum after isolation from rat liver. The photosensitizing efficiency of porphyrin on the Ca# + influx function of microsomes has been compared with that obtained on Ca# + uptake in mitochondria. HP and PP are accumulated in microsomes to a greater extent than in mitochondria, both porphyrins binding to membrane protein sites. The Ca# + influx functions of mitochondria and microsomes, before and after irradiation in the presence of HP or PP, were studied by following the changes in the free Ca# + concentration in the medium as revealed by the variations in fluorescence intensity of the Ca# + indicator Calcium

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Photochemotherapy of Cancer: Experimental Research

Cited by 369 publications

References 220 publications

Bax is essential for mitochondrion-mediated apoptosis but not for cell death caused by photodynamic therapy

Bax is essential for mitochondrion-mediated apoptosis but not for cell death caused by photodynamic therapy

Dissociation of mitochondrial depolarization from cytochrome c release during apoptosis induced by photodynamic therapy

Photodynamic action of porphyrin on Ca2+ influx in endoplasmic reticulum: a comparison with mitochondria

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