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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
Dátum:	2013
ISSN:	1107-3756
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
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001-es BibID:	BIBFORM001035
Első szerző:	Zákány Róza (anatómus-, kötőszövetbiológus)
Cím:	Oxidative stress-induced poly(ADP-ribosyl)ation in chick limb bud-derived chondrocytes / Zákány R., Bakondi E., Juhász T., Matta C., Szíjgyártó Zs., Erdélyi K., Szabó E., Módis L., Virág L., Gergely P.
Dátum:	2007
Megjegyzések:	Oxidative stress has been implicated in the pathogenesisof various diseases affecting chondrogenesis or the function of articular cartilage. DNA damage caused byoxidative stress may trigger the activation of the nuclearenzyme, poly(ADP-ribose) polymerase-1 (PARP-1) whichmay contribute to tissue injury. We aimed at investigating the effects of peroxynitrite (100-600 ?M) and hydrogen peroxide (0.1-4 mM) on PARP activation and extracellular matrix production of high density micromass cultures (HDC)prepared from chick limb bud mesenchymal cells. We foundthat both oxidative species strongly inhibited matrix formation of HDCs treated on day 2 but not on day 5. The PARP inhibitor 3-aminobenzamide (3-AB) stimulated matrix production in non-stressed cells and prevented suppressed matrix production in oxidatively stressed cells. Both hydrogen peroxide and peroxynitrite induced PARP activation and poly(ADP-ribose) accumulation. Decreased proliferation, viability and NAD+ content were not or only slightly improved by 3-AB, indicating that 3-AB directly affects matrix formation. In conclusion, oxidative stress stimulates poly(ADP-ribose) metabolism and inhibits extracellular matrix production of HDCs in a PARP-dependent manner. Our findings may have implications for potential therapeutic approaches aimed at restoring the matrix production capacity of chondrogenic cells.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban poly(ADP-ribosyl)ation oxidative stress peroxynitrite egyetemen (Magyarországon) készült közlemény extracellular matrix chondrocyte
Megjelenés:	International Journal of Molecular Medicine. - 19 : 4 (2007), p. 597-605. -
További szerzők:	Bakondi Edina (1975-) (biokémikus, vegyész) Juhász Tamás (1976-) (biológus, orvosbiológus) Matta Csaba (1980-) (molekuláris biológus, genetikus, angol szakfordító) Szíjgyártó Zsolt (1978-) (vegyész) Erdélyi Katalin (1978-) (molekuláris biológus, biokémikus) Szabó Éva (1965-) (bőrgyógyász, kozmetológus) Módis László (1939-) (anatómus, kötőszövetbiológus) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Gergely Pál (1947-) (biokémikus)
Internet cím:	elektronikus változat elektronikus változat
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