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Two New Faces of Amifostine: Protector from DNA Damage in Normal Cells and Inhibitor of DNA Repair in Cancer Cells
M. Hofer, M. Falk, D. Komůrková, I. Falková, A. Bačíková, B. Klejdus, E. Pagáčová, L. Štefančíková, L. Weiterová, KJ. Angelis, S. Kozubek, L. Dušek, Š. Galbavý,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
Grantová podpora
NV16-29835A
MZ0
CEP - Centrální evidence projektů
- MeSH
- alkalická fosfatasa genetika metabolismus MeSH
- amifostin farmakokinetika farmakologie MeSH
- dvouřetězcové zlomy DNA účinky léků MeSH
- fibroblasty účinky léků účinky záření MeSH
- fluorescenční mikroskopie metody MeSH
- histony genetika metabolismus MeSH
- intracelulární signální peptidy a proteiny genetika metabolismus MeSH
- kometový test MeSH
- lidé MeSH
- merkaptoethylaminy farmakokinetika MeSH
- MFC-7 buňky účinky léků účinky záření MeSH
- oprava DNA účinky léků MeSH
- poškození DNA účinky léků MeSH
- radioprotektivní látky farmakologie MeSH
- záření gama MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Amifostine protects normal cells from DNA damage induction by ionizing radiation or chemotherapeutics, whereas cancer cells typically remain uninfluenced. While confirming this phenomenon, we have revealed by comet assay and currently the most sensitive method of DNA double strand break (DSB) quantification (based on γH2AX/53BP1 high-resolution immunofluorescence microscopy) that amifostine treatment supports DSB repair in γ-irradiated normal NHDF fibroblasts but alters it in MCF7 carcinoma cells. These effects follow from the significantly lower activity of alkaline phosphatase measured in MCF7 cells and their supernatants as compared with NHDF fibroblasts. Liquid chromatography-mass spectrometry confirmed that the amifostine conversion to WR-1065 was significantly more intensive in normal NHDF cells than in tumor MCF cells. In conclusion, due to common differences between normal and cancer cells in their abilities to convert amifostine to its active metabolite WR-1065, amifostine may not only protect in multiple ways normal cells from radiation-induced DNA damage but also make cancer cells suffer from DSB repair alteration.
Citace poskytuje Crossref.org
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- $a Hofer, Michal $u Department of Cell Biology and Radiobiology, Institute of Biophysics, v.v.i., Czech Academy of Sciences , Královopolská 135, CZ-612 65 Brno, Czech Republic.
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- $a Amifostine protects normal cells from DNA damage induction by ionizing radiation or chemotherapeutics, whereas cancer cells typically remain uninfluenced. While confirming this phenomenon, we have revealed by comet assay and currently the most sensitive method of DNA double strand break (DSB) quantification (based on γH2AX/53BP1 high-resolution immunofluorescence microscopy) that amifostine treatment supports DSB repair in γ-irradiated normal NHDF fibroblasts but alters it in MCF7 carcinoma cells. These effects follow from the significantly lower activity of alkaline phosphatase measured in MCF7 cells and their supernatants as compared with NHDF fibroblasts. Liquid chromatography-mass spectrometry confirmed that the amifostine conversion to WR-1065 was significantly more intensive in normal NHDF cells than in tumor MCF cells. In conclusion, due to common differences between normal and cancer cells in their abilities to convert amifostine to its active metabolite WR-1065, amifostine may not only protect in multiple ways normal cells from radiation-induced DNA damage but also make cancer cells suffer from DSB repair alteration.
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- $a Falková, Iva $u Department of Cell Biology and Radiobiology, Institute of Biophysics, v.v.i., Czech Academy of Sciences , Královopolská 135, CZ-612 65 Brno, Czech Republic. Department of Medical Technology, St. Elisabeth University of Health and Social Sciences , Palackého 1, SK-810 00 Bratislava, Slovak Republic.
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