Relationship between photodynamically induced damage to various cellular parameters and loss of clonogenicity in different cell types with hematoporphyrin derivative as sensitizer

Penning, Louis C.; Tijssen, Karmi; Boegheim, J. P. J.; Steveninck, J. Van; Dubbelman, T. M. A. R.

doi:10.1016/0167-4889(94)90248-8

Cited by 15 publications

(8 citation statements)

References 27 publications

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“…Identification of primary photodamage sites can be done by measuring the activities of proteins typical of subcellular organelles immediately after irradiation. The targeted organelles in cell photoinactivation with hematoporphyrin derivative, tetraphenylporphyrins and zinc phthalocyanine have been thus approached (3–6).…”

Section: Introductionmentioning

confidence: 99%

Primary Photodamage Sites and Mitochondrial Events after Foscan® Photosensitization of MCF-7 Human Breast Cancer Cells¶

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Marchal

d'Hallewin

et al. 2007

Photochemistry and Photobiology

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To determine the initial photodamage sites of Foscan®‐mediated photodynamic treatment, we evaluated the enzymatic activities in selected organelles immediately after light exposure of MCF‐7 cells. The measurements indicated that the enzymes located in the Golgi apparatus (uridine 5′‐diphosphate galactosyl transferase) and in the endoplasmic reticulum (ER) (nicotinamide adenine dinucleotide [reduced] [NADH] cytochrome c [cyt c] reductase) are inactivated by the treatment, whereas mitochondrial marker enzymes (cyt c oxidase and dehydrogenases) were unaffected. This indicates that the ER and the Golgi apparatus are the primary intracellular sites damaged by Foscan®‐mediated PDT in MCF‐7 cells. We further investigated whether the specific mitochondria events could be associated with Foscan® photoinduced cell death. The dose response profiles of mitochondrial depolarization and cytochrome c release immediately after Foscan®‐based PDT were very different from that of overall cell death. By 24 h post‐PDT the fluence dependency was strikingly similar for both mitochondrial alterations and cell death. Therefore, although mitochondria are not directly affected by the treatment, they can be strongly implicated in Foscan®‐mediated MCF‐7 cell death by late and indirect mechanism.

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Section: Introductionmentioning

confidence: 99%

Primary Photodamage Sites and Mitochondrial Events after Foscan® Photosensitization of MCF-7 Human Breast Cancer Cells¶

Teiten

Marchal

d'Hallewin

et al. 2007

Photochemistry and Photobiology

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“…This light causes excitation of the photosensitizer, and in this excited state the sensitizer produces singlet oxygen, a cytotoxic form of oxygen, which eradicates tumor cells (Weishaupt et al, 1976). Tumor necrosis is a combined result of direct cell killing (Penning et al, 1994), occlusion of tumor blood vessels (Henderson et al, 1985), and an acute inflammatory reaction (Krosl et al, 1995). PDT has been used to treat many types of cancer, including colon, bladder, lung, esophageal, and head‐and‐neck cancers (Fromm et al, 1996; Nseyo and Lamm, 1996; Furuse et al, 1993; Savary et al, 1997).…”

mentioning

confidence: 99%

Targeting of a hydrophilic photosensitizer by use of internalizing monoclonal antibodies: A new possibility for use in photodynamic therapy

et al. 2000

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Coupling of photosensitizers to tumor‐selective monoclonal antibodies (MAbs) is an attractive option for improving the selectivity of photodynamic therapy (PDT). For this purpose, hydrophilic sensitizers would be most suitable because of their solubility in water. However, such sensitizers are known to be ineffective in PDT, probably because they cannot readily pass the cell membrane and reach the critical intracellular target. We used the model compound TrisMPyP‐ΦCO2H, a hydrophilic porphyrin derivative, to test the hypothesis that hydrophilic photosensitizers might become of therapeutic value when directed into the tumor cell by use of internalizing MAbs. TrisMPyP‐ΦCO2H was conjugated using a labile ester. Conjugates showed no impairment of integrity on SDS‐PAGE, full stability in serum in vitro, and optimal immunoreactivity when the sensitizer:MAb ratio was ≤3. At higher molar ratios, the solubility of the conjugates decreased. In vitro internalization experiments showed that TrisMPyP‐ΦCONH–125I‐cMAb U36 and TrisMPyPΦCONH–125I‐mMAb 425 conjugates were internalized by A431 cells, in contrast to TrisMPyP‐ΦCONH–125I‐mMAb E48 conjugates. Data on the in vitro efficacy of PDT with MAb‐conjugated TrisMPyP‐ΦCO2H showed that the internalizing cMAb U36 and mMAb 425 conjugates were phototoxic to A431 cells, while the non‐internalizing E48 conjugate and the unconjugated sensitizer were not. Biodistribution data of conjugates with sensitizer:125I‐cMAb U36 ratios varying from 1:1 to 3:1 in tumor‐bearing nude mice revealed selective accumulation in the tumor. Conjugates with higher molar ratios were cleared more rapidly from the blood than the unconjugated 125I‐cMAb U36, resulting in lower tumor uptake but similar tumor‐to‐blood ratios. Our data suggest that hydrophilic photosensitizers might have therapeutic value when targeted to tumors by internalizing MAbs. Int. J. Cancer 88:108–114, 2000. © 2000 Wiley‐Liss, Inc.

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“…Being hydrophobic in character, HPD tends to localize in plasma and subcellular membranes, making these structures especially sensitive to the photooxidative damage. Namely, it was reported that photodynamic treatment of tumour cells with HPD induces extensive alterations in the cell morphology (Volden et al, 1981), inhibits various membrane transport systems (Penning et al, 1994), destructs cellular membranes and mitochondria (Tatsuta et al, 1984). Moreover, among the subcellular organelles mitochondria are considered to be critical targets for the cell killing induced by photoactivated HPD (Hilf et al, 1986;Oleinick et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

“…There are some indications that cellular proteins are very sensitive to the photodynamic action of HPD. It was reported that photosensitization of tumour cells by HPD may cross-link membranous proteins (Moan & Vistnes, 1986), decrease the activity of various enzymes (Hilf et al, 1986;Atlante et al, 1989;Gibson et al, 1989;Prinsze et al, 1991), and affect the Na + /K + -ATPase pump (Penning et al, 1994). Moreover, it was shown (Moan & Vistnes, 1986) that in tumour cells a significant fraction of the photodrug is in close contact with proteins.…”

Section: Introductionmentioning

confidence: 99%

On the mechanism of cellular death under photoexcitation of haematoporphyrin derivative

Chekulayev¹,

Chekulayeva²,

Shevchuk³

2003

Proceedings of the Estonian Academy of Sciences. Biology. Ecolo

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Relationship between photodynamically induced damage to various cellular parameters and loss of clonogenicity in different cell types with hematoporphyrin derivative as sensitizer

Cited by 15 publications

References 27 publications

Primary Photodamage Sites and Mitochondrial Events after Foscan® Photosensitization of MCF-7 Human Breast Cancer Cells¶

Primary Photodamage Sites and Mitochondrial Events after Foscan® Photosensitization of MCF-7 Human Breast Cancer Cells¶

Targeting of a hydrophilic photosensitizer by use of internalizing monoclonal antibodies: A new possibility for use in photodynamic therapy

On the mechanism of cellular death under photoexcitation of haematoporphyrin derivative

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