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Effects of Zinc Phthalocyanine Photodynamic Therapy on Vital Structures and Processes in Hela Cells
J. Hosik, B. Hosikova, S. Binder, R. Lenobel, M. Kolarikova, L. Malina, H. Dilenko, K. Langova, R. Bajgar, H. Kolarova
Language English Country Switzerland
Document type Journal Article
Grant support
NU21J-03-00062
The Ministry of Health Czech Republic
NLK
Free Medical Journals
from 2000
Freely Accessible Science Journals
from 2000
PubMed Central
from 2007
Europe PubMed Central
from 2007
ProQuest Central
from 2000-03-01
Open Access Digital Library
from 2000-01-01
Open Access Digital Library
from 2007-01-01
Health & Medicine (ProQuest)
from 2000-03-01
ROAD: Directory of Open Access Scholarly Resources
from 2000
PubMed
39408981
DOI
10.3390/ijms251910650
Knihovny.cz E-resources
- MeSH
- Photochemotherapy * methods MeSH
- Photosensitizing Agents * pharmacology chemistry MeSH
- HeLa Cells MeSH
- Indoles * pharmacology chemistry MeSH
- Isoindoles * MeSH
- Humans MeSH
- Membrane Potential, Mitochondrial * drug effects MeSH
- Organometallic Compounds * pharmacology chemistry MeSH
- Oxidative Stress drug effects MeSH
- DNA Damage drug effects MeSH
- Reactive Oxygen Species * metabolism MeSH
- Zinc Compounds * pharmacology MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
This work presents results on the efficiency of newly designed zinc phthalocyanine-mediated photodynamic therapy of both tumoral and nontumoral cell models using the MTT assay. Further detailed examinations of mechanistic and cell biological effects were focused on the HELA cervical cancer cell model. Here, ROS production, changes in the mitochondrial membrane potential, the determination of genotoxicity, and protein changes determined by capillary chromatography and tandem mass spectrometry with ESI were analyzed. The results showed that, in vitro, 5 Jcm-2 ZnPc PDT caused a significant increase in reactive oxygen species. Still, except for superoxide dismutase, the levels of proteins involved in cell response to oxidative stress did not increase significantly. Furthermore, this therapy damaged mitochondrial membranes, which was proven by a more than 70% voltage-dependent channel protein 1 level decrease and by a 65% mitochondrial membrane potential change 24 h post-therapy. DNA impairment was assessed by an increased level of DNA fragmentation, which might be related to the decreased level of DDB1 (decrease in levels of more than 20% 24 h post-therapy), a protein responsible for maintaining genomic integrity and triggering the DNA repair pathways. Considering these results and the low effective concentration (LC50 = 30 nM), the therapy used is a potentially very promising antitumoral treatment.
References provided by Crossref.org
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