Effect of carvedilol on the production of reactive oxygen species by HL-60 cells
Jazyk angličtina Země Švédsko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
18987604
PII: NEL290508A18
Knihovny.cz E-zdroje
- MeSH
- adenosintrifosfát metabolismus MeSH
- beta blokátory farmakologie toxicita MeSH
- buněčná diferenciace účinky léků MeSH
- fagocyty účinky léků MeSH
- fluorometrie MeSH
- granulocyty účinky léků MeSH
- HL-60 buňky MeSH
- karbazoly farmakologie toxicita MeSH
- karvedilol MeSH
- lidé MeSH
- luminiscence MeSH
- oxid dusnatý metabolismus MeSH
- peroxidy metabolismus MeSH
- proliferace buněk účinky léků MeSH
- propanolaminy farmakologie toxicita MeSH
- reaktivní formy kyslíku metabolismus MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- adenosintrifosfát MeSH
- beta blokátory MeSH
- karbazoly MeSH
- karvedilol MeSH
- oxid dusnatý MeSH
- peroxidy MeSH
- propanolaminy MeSH
- reaktivní formy kyslíku MeSH
OBJECTIVES: The generation of reactive oxygen species (ROS) by phagocytes is one of the irreplaceable microbicidal tools of innate immunity. It has been reported in our previous studies that short-term treatment by carvedilol ex vivo inhibits ROS generation. The purpose of this study was to investigate the long-term effect of carvedilol on phagocytes. METHODS: Human leukemia HL-60 cells differentiated into granulocyte-like cells were used as the model. Final concentrations of carvedilol were 0.1-100 micromol/l. The production of ROS by HL-60 cells was measured using luminol-enhanced chemiluminescence (CL). RESULTS: Carvedilol in concentrations 0.1-10 micromol/l did not exhibit any toxic effect on cells (measured using bioluminescent bacteria Photorhabdus luminescens subsp. thracensis). One hour's treatment with 10 micromol/l carvedilol significantly decreased both spontaneous and activated CL of cells. Conversely, no inhibitory effects on CL were observed in 10 micromol/l carvedilol after 48 h incubation; lower concentrations of carvedilol even slightly increased the CL activity of HL-60 cells. A significant increase in spontaneous CL activity was detected in cells incubated with 10 micromol/l carvedilol in comparison with the control. Powerful antioxidative properties of carvedilol against peroxyl radical (ORAC assay) were proved. No scavenging of nitric oxide (electrochemical method) was observed. CONCLUSIONS: Long-term influence of carvedilol can induce an increase in the generation of phagocyte-derived ROS and potentially also other inflammatory mediators. The increased ROS production is compensated for by antioxidative properties of carvedilol although the increased production of inflammatory mediators could affect the proper function of immune system.