Összesen 4 találat.


001-es BibID:BIBFORM001037
Első szerző:Bai Péter (biokémikus)
Cím:Protein tyrosine nitration and poly(ADP-ribose) polymerase activation in N-methyl-N-nitrosoguanidine-treated thymocytes : implication for cytotoxicity / Bai P., Hegedűs C., Erdélyi K., Szabó E., Bakondi E., Gergely S., Szabó C., Virág L.
Megjegyzések:1-Methyl-3-nitro-1-nitrosoguanidine (MNNG) is a DNA alkylating agent. DNA alkylation by MNNG is known to trigger accelerated poly(ADP-ribose) metabolism. Various nitroso compounds release nitric oxide (NO). Therefore, we set out to investigate whether MNNG functions as NO donor and whether MNNG-derived NO or secondary NO metabolites such as peroxynitrite contribute to MNNG-induced cytotoxicity. MNNG in aqueous solutions resulted in time- and concentration-dependent NO release and nitrite/nitrate formation. Moreover, various proteins in MNNG-treated thymocytes were found to be nitrated, indicating that MNNG-derived NO may combine with cellular superoxide to form peroxynitrite, a nitrating agent. MNNG also caused DNA breakage and increased poly(ADP-ribose) polymerase activity and cytotoxicity in thymocytes. MNNG-induced DNA damage (measured by the comet assay) and thymocyte death (measured by propidium iodide uptake) was prevented by the PARP inhibitor PJ-34 and by glutathione (GSH) or N-acetylcysteine (NAC). The cytoprotection provided by PJ-34 against necrotic parameters was paralleled by increased outputs in apoptotic parameters (caspase activity, DNA laddering) indicating that PARP activation diverts apoptotic death toward necrosis. As MNNG-induced cytotoxicity showed many similarities to peroxynitrite-induced cell death, we tested whether peroxynitrite was responsible for at least part of the cytotoxicity induced by MNNG. Cell-permeable enzymic antioxidants (superoxide dismutase and catalase), the NO scavenger cPTIO or the peroxynitrite decomposition catalyst FP15 failed to inhibit MNNG-induced DNA breakage and cytotoxicity. In conclusion, MNNG induces tyrosine nitration in thymocytes. Furthermore, MNNG damages DNA by a radical mechanism that does not involve NO or peroxynitrite.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
poly(ADP-ribose) polymerase
nitric oxide
Megjelenés:Toxicology Letters 170 : 3 (2007), p. 203-213. -
További szerzők:Hegedűs Csaba (1980-) (biokémikus, molekuláris biológus) Erdélyi Katalin (1978-) (molekuláris biológus, biokémikus) Szabó Éva (1965-) (bőrgyógyász, kozmetológus) Bakondi Edina (1975-) (biokémikus, vegyész) Gergely Szabolcs (1977-) (kardiológus) Szabó Csaba Virág László (1965-) (biokémikus, sejtbiológus, farmakológus)
Internet cím:elektronikus változat


001-es BibID:BIBFORM014285
Első szerző:Bakondi Edina (biokémikus, vegyész)
Cím:Cytoprotective effect of gallotannin in oxidatively stressed HaCaT keratinocytes : the role of poly(ADP-ribose) metabolism / Edina Bakondi, Péter Bai, Katalin Erdélyi, Csaba Szabó, Pál Gergely, László Virág
ISSN:0891-5849 (Print)
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Astringents/ pharmacology
Cell Line
Hydrolyzable Tannins/ pharmacology
Keratinocytes/cytology/drug effects/ metabolism
Oxidative Stress/drug effects
Poly(ADP-ribose) Polymerases/ metabolism
Asthma/ drug therapy
Bronchoalveolar Lavage
Cell Death
Cell Movement
Chemokine CXCL2
Disease Models, Animal
Enzyme Inhibitors/ pharmacology
Leukocytes, Mononuclear/metabolism
Mice, Inbred BALB C
Poly(ADP-ribose) Polymerases/ antagonists & inhibitors
Time Factors
Tumor Necrosis Factor-alpha/metabolism
Antineoplastic Agents/toxicity
Biological Markers/analysis
Cardiomyopathy, Dilated/chemically induced/enzymology
Doxorubicin/ toxicity
Enzyme Activation
Heart/ drug effects
Heart Failure/chemically induced
Matrix Metalloproteinases/ metabolism
Models, Animal
Myocardium/enzymology/ pathology
Reperfusion Injury/chemically induced/enzymology
Acute Disease
Catalysis/drug effects
Chronic Disease
Creatine Kinase/blood
Enzyme Inhibitors/pharmacology
Heart/ drug effects/physiopathology
Heart Failure/ chemically induced/physiopathology/prevention & control
L-Lactate Dehydrogenase/blood
Metalloporphyrins/ pharmacology
Mice, Inbred C57BL
Mice, Knockout
Nitric Oxide Synthase/antagonists & inhibitors/genetics/metabolism
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
Oxidative Stress/drug effects/genetics
Peroxynitrous Acid/ metabolism
Survival Rate
Antibiotics, Antineoplastic
Creatine Kinase/metabolism
Enzyme Activation/drug effects
Heart Failure/ chemically induced/pathology/physiopathology
Hemodynamics/drug effects
L-Lactate Dehydrogenase/metabolism
Poly(ADP-ribose) Polymerases/ genetics/ metabolism
Survival Analysis
Ventricular Function, Left/genetics
Benzamides/ pharmacology
Cells, Cultured
DNA Damage/drug effects
DNA Fragmentation/drug effects
Enzyme Activation/drug effects/physiology
Mitochondria/ drug effects
Nitrogen Oxides/ toxicity
Poly(ADP-ribose) Polymerases/ antagonists & inhibitors/metabolism
Protective Agents/ pharmacology
Thymus Gland/cytology/ drug effects
Megjelenés:Experimental Dermatology 13 : 3 (2004), p. 170-178. -
További szerzők:Bai Péter (1976-) (biokémikus) Erdélyi Katalin (1978-) (molekuláris biológus, biokémikus) Szabó Csaba Gergely Pál (1947-) (biokémikus) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
elektronikus változat


001-es BibID:BIBFORM048850
035-os BibID:PMID:23722590
Első szerző:Erdélyi Katalin (molekuláris biológus, biokémikus)
Cím:Role of poly(ADP-ribosyl)ation in a 'two-hit' model of hypoxia and oxidative stress in human A549 epithelial cells in vitro / Katalin Erdélyi, Pál Pacher, László Virág, Csaba Szabó
Megjegyzések:A preceding hypoxic insult can sensitize the cells or the organism to a subsequent, second insult. The aim of the present study was to investigate the molecular mechanism of this phenomenon (often termed 'two-hit' injury paradigm), in an in vitro model of hypoxia/oxidative stress injury in A549 epithelial cells, with special emphasis on the role of the nuclear enzyme poly(ADP-ribose) polymerase-1 (PARP-1) in the process. Pre-exposure of the cells to 24 h hypoxia significantly reduced intracellular glutathione (GSH) levels, reduced mitochondrial activity and adenosine triphosphate (ATP) levels. However pre-exposure to hypoxia failed to induce any change in PARP-1 expression and activation, DNA single-strand breaks or plasma membrane integrity. Pre-exposure to hypoxia markedly increased the sensitivity of the cells to subsequent oxidative stress-induced DNA damage. Hydrogen peroxide (H2O2) induced a concentration-dependent increase in DNA breakage, PARP activation, depletion of intracellular ATP, inhibition of mitochondrial activity and two distinct parameters that quantify the breakdown of plasma membrane integrity (propidium iodide uptake or lactate dehydrogenase release). PARP-1 activation played a significant role in the H2O2-induced cell death response because PARP activation, depletion of intracellular ATP, inhibition of mitochondrial activity, and the breakdown of plasma membrane integrity were attenuated in cells with permanently silenced PARP-1. Based on measurement of the endogenous antioxidant GSH, we hypothesized that the mechanism of hypoxia-mediated enhancement of H2O2 involves depletion of the GSH during the hypoxic period, which renders the cells more sensitive to a subsequent DNA single-strand break elicited by H2O2. DNA strand breakage then activates PARP-1, leading to the inhibition of mitochondrial function, depletion of ATP and cell necrosis. PARP-1 deficiency protects against the cytotoxicity, to a lesser degree, by protecting against GSH depletion during the hypoxic period, and, to a larger degree, by maintaining mitochondrial function and preserving intracellular ATP levels during the subsequent oxidative stress period.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:International Journal of Molecular Medicine. - 32 : 2 (2013), p. 339-346. -
További szerzők:Pacher Pál Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Szabó Csaba
Internet cím:Szerző által megadott URL
Intézményi repozitóriumban (DEA) tárolt változat


001-es BibID:BIBFORM007444
Első szerző:Erdélyi Katalin (molekuláris biológus, biokémikus)
Cím:Dual role of poly(ADP-ribose) glycohydrolase in the regulation of cell death in oxidatively stressed A549 cells / Erdélyi K., Bai P., Kovács I., Szabó É., Mocsár G., Kakuk A., Szabó Cs., Gergely P., Virág L.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
DNA damage
gene silencing
egyetemen (Magyarországon) készült közlemény
hydrogen peroxide
apoptosis-inducing factor
Megjelenés:The FASEB Journal. - 23 : 10 (2009), p. 3553-3563. -
További szerzők:Bai Péter (1976-) (biokémikus) Kovács István (1985-) (biokémikus) Szabó Éva (1965-) (bőrgyógyász, kozmetológus) Mocsár Gábor (1981-) (biofizikus) Kakuk Annamária (1976-) (molekuláris biológus) Szabó Csaba Gergely Pál (1947-) (biokémikus) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus)
Internet cím:elektronikus változat
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