-
Something wrong with this record ?
High glucose increases susceptibility to oxidative-stress-induced apoptosis and DNA damage in K-5612 cells
Jan Hruda, Vladimir Sramek, Xavier Leverve
Language English Country Czech Republic
NLK
Directory of Open Access Journals
from 2001
Free Medical Journals
from 1998
Medline Complete (EBSCOhost)
from 2007-06-01
ROAD: Directory of Open Access Scholarly Resources
from 2001
- MeSH
- Acetylcysteine pharmacology MeSH
- Antioxidants pharmacology MeSH
- Apoptosis MeSH
- K562 Cells physiology drug effects MeSH
- Financing, Organized MeSH
- Fructose pharmacology MeSH
- Glucose administration & dosage MeSH
- Glutamine pharmacology MeSH
- Humans MeSH
- Oxidative Stress MeSH
- Hydrogen Peroxide pharmacology MeSH
- DNA Damage MeSH
- Drug Synergism MeSH
- tert-Butylhydroperoxide pharmacology MeSH
- Dose-Response Relationship, Drug MeSH
- Check Tag
- Humans MeSH
Aim. The study was carried out to evaluate the effect of several substrates on oxidative stress induced apoptosis and in K-562 cells. Methods. Glucose at 5, 11 and 30 mM concentrations was tested, as well as 5 mM glutamine and 5 mM fructose. The cells were exposed to tert-butylhydroperoxide (tBH) and apoptotic cells were evaluated by flow cytometry with FITC-Annexin V and propidium iodide. The effect of glucose concentration on DNA damage was evaluated using hydrogen peroxide and electrophoretic “DNA comets” assay at 5 mM and 30 mM glucose concentrations. Results. The exposure of cells to tBH resulted in increased number of apoptotic cells, and this effect was prevented by administration of an antioxidant – N-Acetyl cysteine. Rising concentrations of glucose added to the toxic effect of tBH; we also observed some toxic effect of fructose and no effect of glutamine. We found higher susceptibility to hydrogen peroxide induced DNA damage with 30 mM glucose concentration. Conclusion. Hyperglycemia increases the cell’s susceptibility to oxidative stress and it also amplifies oxidative DNA damage. Glutamine – when used as a sole energetic substrate – showed no protective effect against oxidative stress.
Lit.: 16
- 000
- 00000naa 2200000 a 4500
- 001
- bmc11002139
- 003
- CZ-PrNML
- 005
- 20111210201936.0
- 008
- 110220s2010 xr e eng||
- 009
- AR
- 040 __
- $a ABA008 $b cze $c ABA008 $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xr
- 100 1_
- $a Hruda, Jan. $7 xx0230395
- 245 10
- $a High glucose increases susceptibility to oxidative-stress-induced apoptosis and DNA damage in K-5612 cells / $c Jan Hruda, Vladimir Sramek, Xavier Leverve
- 314 __
- $a Department of Anaesthesia and Intensive Care, St. Anne's University Hospital, Masaryk University, Brno
- 504 __
- $a Lit.: 16
- 520 9_
- $a Aim. The study was carried out to evaluate the effect of several substrates on oxidative stress induced apoptosis and in K-562 cells. Methods. Glucose at 5, 11 and 30 mM concentrations was tested, as well as 5 mM glutamine and 5 mM fructose. The cells were exposed to tert-butylhydroperoxide (tBH) and apoptotic cells were evaluated by flow cytometry with FITC-Annexin V and propidium iodide. The effect of glucose concentration on DNA damage was evaluated using hydrogen peroxide and electrophoretic “DNA comets” assay at 5 mM and 30 mM glucose concentrations. Results. The exposure of cells to tBH resulted in increased number of apoptotic cells, and this effect was prevented by administration of an antioxidant – N-Acetyl cysteine. Rising concentrations of glucose added to the toxic effect of tBH; we also observed some toxic effect of fructose and no effect of glutamine. We found higher susceptibility to hydrogen peroxide induced DNA damage with 30 mM glucose concentration. Conclusion. Hyperglycemia increases the cell’s susceptibility to oxidative stress and it also amplifies oxidative DNA damage. Glutamine – when used as a sole energetic substrate – showed no protective effect against oxidative stress.
- 650 _2
- $a financování organizované $7 D005381
- 650 _2
- $a acetylcystein $x farmakologie $7 D000111
- 650 _2
- $a antioxidancia $x farmakologie $7 D000975
- 650 _2
- $a apoptóza $7 D017209
- 650 _2
- $a poškození DNA $7 D004249
- 650 _2
- $a vztah mezi dávkou a účinkem léčiva $7 D004305
- 650 _2
- $a synergismus léků $7 D004357
- 650 _2
- $a fruktosa $x farmakologie $7 D005632
- 650 _2
- $a glukosa $x aplikace a dávkování $7 D005947
- 650 _2
- $a glutamin $x farmakologie $7 D005973
- 650 _2
- $a lidé $7 D006801
- 650 _2
- $a peroxid vodíku $x farmakologie $7 D006861
- 650 _2
- $a buňky K562 $x fyziologie $x účinky léků $7 D020014
- 650 _2
- $a oxidační stres $7 D018384
- 650 _2
- $a terc-butylhydroperoxid $x farmakologie $7 D020122
- 700 1_
- $a Šrámek, Vladimír, $d 1958- $7 xx0002872
- 700 1_
- $a Leverve, Xavier
- 773 0_
- $w MED00012606 $t Biomedical papers $g Roč. 154, č. 4 (2010), s. 315-320 $x 1213-8118
- 856 41
- $u http://biomed.papers.upol.cz/pdfs/bio/2010/04/07.pdf $y plný text volně přístupný
- 910 __
- $a ABA008 $b A 1502 $c 958 $y 2
- 990 __
- $a 20110219071424 $b ABA008
- 991 __
- $a 20110725120931 $b ABA008
- 999 __
- $a ok $b bmc $g 829391 $s 694093
- BAS __
- $a 3
- BMC __
- $a 2010 $b 154 $c 4 $d 315-320 $m Biomedical papers of the Medical Faculty of the University Palacký, Olomouc Czech Republic $x MED00012606
- LZP __
- $a 2011-11/ipme