Ca(2+)-mediated prostaglandin E2 induction reduces haematoporphyrin-derivative-induced cytotoxicity of T24 human bladder transitional carcinoma cells in vitro
| Autor: | Louis C. Penning, John VanSteveninck, M J N C Keirse, Tom M.A.R. Dubbelman |
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| Jazyk: | angličtina |
| Rok vydání: | 1993 |
| Předmět: |
medicine.medical_specialty
Cell Survival Pharmacology Biochemistry Dinoprostone chemistry.chemical_compound Phospholipase A2 Internal medicine Extracellular medicine Tumor Cells Cultured Humans Hematoporphyrin Derivative Prostaglandin E2 Cytotoxicity Molecular Biology Carcinoma Transitional Cell biology Cell Biology Thromboxane B2 EGTA Cell killing Endocrinology chemistry Photochemotherapy Urinary Bladder Neoplasms biology.protein lipids (amino acids peptides and proteins) Calcium Intracellular medicine.drug Research Article |
| Popis: | The effects of haematoporphyrin-derivative-mediated photodynamic treatment on arachidonic acid metabolism and its relation to clonogenicity have been studied in human bladder-tumour cells. Photodynamic treatment resulted in a transient release of arachidonic acid-derived compounds; prostaglandin E2 (PGE2) and thromboxane B2 (TXB2) especially were strongly increased. This release was reduced by chelation of intracellular Ca2+ with Quin-2 or by lowering the extracellular Ca2+ concentration in the medium with EGTA, presumably resulting in inhibition of phospholipase A2. A similar reduction was obtained when indomethacin, an inhibitor of the cyclo-oxygenase pathway, was added prior to light exposure. These three treatments enhanced the photosensitivity, as revealed by the clonogenicity assay. Incubation with PGE2 prior to light exposure, but not with TXB2, protected against reproductive-cell death. The results of these experiments suggest that Ca(2+)-mediated activation of cyclo-oxygenase, resulting in increased levels of PGE2, participates in a cellular-defence mechanism against photodynamic cell killing. |
| Databáze: | OpenAIRE |
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