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1.

001-es BibID:BIBFORM048678
035-os BibID:PMID:23290998
Első szerző:Bürkle, Alexander
Cím:Poly(ADP-ribose) : PARadigms and PARadoxes / Alexander Bürkle, László Virág
Dátum:2013
ISSN:0098-2997 1872-9452
Megjegyzések:Poly(ADP-ribosyl)ation (PARylation) is a posttranslational protein modification (PTM) catalyzed by members of the poly(ADP-ribose) polymerase (PARP) enzyme family. PARPs use NAD(+) as substrate and upon cleaving off nicotinamide they transfer the ADP-ribosyl moiety covalently to suitable acceptor proteins and elongate the chain by adding further ADP-ribose units to create a branched polymer, termed poly(ADP-ribose) (PAR), which is rapidly degraded by poly(ADP-ribose) glycohydrolase (PARG) and ADP-ribosylhydrolase 3 (ARH3). In recent years several key discoveries changed the way we look at the biological roles and mode of operation of PARylation. These paradigm shifts include but are not limited to (1) a single PARP enzyme expanding to a PARP family; (2) DNA-break dependent activation extended to several other DNA dependent and independent PARP-activation mechanisms; (3) one molecular mechanism (covalent PARylation of target proteins) underlying the biological effect of PARPs is now complemented by several other mechanisms such as protein-protein interactions, PAR signaling, modulation of NAD(+) pools and (4) one principal biological role in DNA damage sensing expanded to numerous, diverse biological functions identifying PARP-1 as a real moonlighting protein. Here we review the most important paradigm shifts in PARylation research and also highlight some of the many controversial issues (or paradoxes) of the field such as (1) the mostly synergistic and not antagonistic biological effects of PARP-1 and PARG; (2) mitochondrial PARylation and PAR decomposition, (3) the cross-talk between PARylation and signaling pathways (protein kinases, phosphatases, calcium) and the (4) divergent roles of PARP/PARylation in longevity and in age-related diseases.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Apoptosis
Calcium
Cell death
Chromatin structure
DNA repair
Kinase
Mitochondria
Necrosis
Poly(ADP-ribose) glycohydrolase
Poly(ADP-ribose) polymerase
Signaling
Transcription
Molekuláris Medicina
Megjelenés:Molecular Aspects of Medicine. - 34 : 6 (2013), p. 1046-1065. -
További szerzők:Virág László (1965-) (biokémikus, sejtbiológus, farmakológus)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Oxidatív stressz és ADP-riboziláció kapcsolatának vizsgálata
TÁMOP-4.2.2.A-11/1/KONV-2012-0025
TÁMOP
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2.

001-es BibID:BIBFORM087277
Első szerző:Douida, Abdennour
Cím:The proteasome activator PA200 regulates expression of genes involved in cell survival upon selective mitochondrial inhibition in neuroblastoma cells / Abdennour Douida, Frank Batista, Agnieszka Robaszkiewicz, Pal Boto, Azzam Aladdin, Mónika Szenykiv, Rita Czinege, László Virág, Krisztina Tar
Dátum:2020
ISSN:1582-1838 1582-4934
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Journal Of Cellular And Molecular Medicine. - 24 : 12 (2020), p. 6716-6730. -
További szerzők:Batista, Frank (1975-) (biokémikus) Robaszkiewicz, Agnieszka (1983-) (biokémikus) Botó Pál (1986-) (molekuláris biológus) Aladdin, Azzam (1980-) (molekuláris biológus) Szenykiv Mónika Czinege Rita Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Tar Krisztina (1975-) (biokémikus, molekuláris biológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00020
GINOP
GINOP-2.3.2-15-2016-00048
GINOP
OTKA K112336
OTKA
OTKA K132193
OTKA
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3.

001-es BibID:BIBFORM054756
Első szerző:El-Hamoly, Tarek
Cím:Activation of poly(ADP-ribose) polymerase-1 delays wound healing by regulating keratinocyte migration and production of inflammatory mediators / Tarek El-Hamoly, Csaba Hegedűs, Petra Lakatos, Katalin Kovács, Péter Bai, Mona A. El-Ghazaly, Ezzeddin S. El-Denshary, Éva Szabó, László Virág
Dátum:2014
ISSN:1076-1551
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Molecular Medicine. - 20 (2014), p. 363-371. -
További szerzők:Hegedűs Csaba (1980-) (biokémikus, molekuláris biológus) Lakatos Petra (1985-) (Molekuláris biológus) Kovács Katalin (1978-) (biokémikus) Bai Péter (1976-) (biokémikus) El-Ghazaly, Mona A. El-Denshary, Ezzeddin S. Szabó Éva (1965-) (bőrgyógyász, kozmetológus) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus)
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4.

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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5.

001-es BibID:BIBFORM057006
Első szerző:Kiss Borbála Katalin (bőrgyógyász, onkológus)
Cím:Poly(ADP) ribose polymerase-1 ablation alters eicosanoid and docosanoid signaling and metabolism in a murine model of contact hypersensitivity / Borbála Kiss, Magdolna Szántó, Mónika Szklenár, Attila Brunyánszki, Tamás Marosvölgyi, Eszter Sárosi, Éva Remenyik, Pál Gergely, László Virág, Tamás Decsi, Ralph Rühl, Peter Bai
Dátum:2015
ISSN:1791-2997 1791-3004
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Molecular Medicine Reports. - 11 : 4 (2015), p. 2861-2867. -
További szerzők:Szántó Magdolna (1984-) (gyógyszerész) Szklenár Mónika Brunyánszki Attila (1980-) (biológus, biotechnológus) Marosvölgyi Tamás Sárosi Eszter Remenyik Éva (1956-) (bőrgyógyász) Gergely Pál (1947-) (biokémikus) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Decsi Tamás Rühl, Ralph (1969-) (vegyész) Bai Péter (1976-) (biokémikus)
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6.

001-es BibID:BIBFORM028371
Első szerző:Komjáti Katalin
Cím:Poly(ADP-ribose) polymerase inhibition protect neurons and the white matter and regulates the translocation of apoptosis-inducing factor in stroke / Katalin Komjáti, John G. Mabley, László Virág, Garry J. Southan, Andrew L. Salzman, Csaba Szabó
Dátum:2004
ISSN:1107-3756
Megjegyzések:Focal cerebral ischemia activates the nuclear protein poly(ADP-ribose) polymerase (PARP). Apoptosis-inducing factor (AIF) is a flavoprotein that is normally confined to the mitochondria, but translocates to the nucleus, as shown by in vitro models of neuronal injury. Using INO-1001, a novel potent inhibitor of PARP, we determined the role of PARP activation in the process of AIF translocation in a rat model of focal cerebral ischemia. The potency of INO-1001 as a PARP inhibitor and its cytoprotective potential in oxidant-challenged human neuronal SK-N-MC cells was first confirmed in vitro. PARP inhibition markedly reduced infarct size and improved neurological status in both transient and permanent models of MCA occlusion in Sprague-Dawley rats, with a therapeutic window of 6 h and 2 h in the transient and permanent ischemia models, respectively. The PARP inhibitor reduced the accumulation of poly(ADP-ribose) in the ischemic/reperfused hemisphere and reduced the accumulation of APP in the white matter of the affected hemisphere, consistently with protection against neuronal necrosis and axonal damage, respectively. Immunohistochemical analysis showed the appearance of AIF labeling in neuronal nuclei of the border zone ischemic area in the striatum after stroke. Cytoplasmatic (axonal) AIF staining was significantly diminished in the necrotic core of the striatum, while it was somewhat enhanced at the borderline ischemic territories of the white matter. Inhibition of PARP with INO-1001 reshifted the location of the apoptotic marker to the axons in the ipsilateral striatum. Thus, PARP inhibition is neuroprotective and regulates the ischemic nuclear translocation of AIF in stroke.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:International Journal Of Molecular Medicine 13 : 3 (2004), p. 373-382. -
További szerzők:Mabley, Jon G. Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Southan, Garry J. Salzman, Andrew L. Szabó Csaba (1967-) (orvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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7.

001-es BibID:BIBFORM028390
Első szerző:Soriano, Francisco Garcia
Cím:Diabetic endothelial dysfunction : role of reactive oxygen and nitrogen species production and poly(ADP-ribose) polymerase activation / Francisco Garcia Soriano, László Virág, Csaba Szabó
Dátum:2001
ISSN:0946-2716
Megjegyzések:Peroxynitrite and hydroxyl radicals are potent initiators of DNA single-strand breakage, which is an obligatory stimulus for the activation of the nuclear enzyme poly(ADP ribose) polymerase (PARP). In response to high glucose incubation medium in vitro, or diabetes and hyperglycemia in vivo, reactive nitrogen and oxygen species generation occurs. These reactive species trigger DNA single-strand breakage, which induces rapid activation of PARP. PARP in turn depletes the intracellular concentration of its substrate, NAD+, slowing the rate of glycolysis, electron transport, and ATP formation. This process results in acute endothelial dysfunction in diabetic blood vessels. Accordingly, inhibitors of PARP protect against endothelial injury under these conditions. In addition to the direct cytotoxic pathway regulated by DNA injury and PARP activation, PARP also appears to modulate the course of inflammation by regulating the activation of nuclear factor kappaB, and the expression of a number of genes, including the gene for intercellular adhesion molecule 1 and the inducible nitric oxide synthase. The research into the role of PARP in diabetic vascular injury is now supported by novel tools, such as new classes of potent inhibitors of PARP and genetically engineered animals lacking the gene for PARP. Pharmacological inhibition of PARP emerges as a potential approach for the experimental therapy of diabetic vascular dysfunction.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
free radicals
oxidatns
nitric oxide
diabetes vascular
cytokine
egyetemen (Magyarországon) készült közlemény
Megjelenés:Journal of Molecular Medicine 79 : 8 (2001), p. 437-448. -
További szerzők:Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Szabó Csaba (1967-) (orvos)
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8.

001-es BibID:BIBFORM028551
Első szerző:Szabó Csaba (orvos)
Cím:Part I : pathogenetic role of peroxynitrite in the development of diabetes and diabetic vascular complications : studies with FP15, a novel potent peroxynitrite decomposition catalyst / Csaba Szabó, Jon G. Mabley, Suzanne M. Moeller, Roman Shimanovich, Pál Pacher, László Virág, Francisco G. Soriano, John H. Van Duzer, William Williams, Andrew L. Salzman, John T. Groves
Dátum:2002
ISSN:1076-1551
Megjegyzések:BACKGROUND: Peroxynitrite is a cytotoxic oxidant formed from nitric oxide (NO) and superoxide. Tyrosine nitration, a footprint of peroxynitrite, has been demonstrated in the pancreatic islets as well as in the cardiovascular system of diabetic subjects. Delineation of the pathogenetic role of peroxynitrite in disease conditions requires the use of potent, in vivo active peroxynitrite decomposition catalysts. The aim of the current work was to produce a potent peroxynitrite decomposition catalyst and to test its effects in rodent models of diabetes and its complications. METHODS: FP15 was synthesized and analyzed using standard chemical methods. Diabetes was triggered by the administration of streptozotocin. Tyrosine nitration was measured immunohistochemically. Cardiovascular and vascular measurements were conducted according to standard physiologic methods. RESULTS: FP15, a potent porphyrinic peroxynitrite decomposition catalyst, potently inhibited tyrosine nitration and peroxynitrite-induced cytotoxicity in vitro and in vivo. FP15 treatment (3-10 mg/kg/d) dose dependently and reduced the incidence and severity of diabetes mellitus in rats subjected to multiple low doses of streptozotocin, as well as in nonobese mice developing spontaneous autoimmune diabetes. Furthermore, treatment with FP15 protected against the development of vascular dysfunction (loss of endothelium-dependent relaxations) and the cardiac dysfunction (loss of myocardial contractility) in diabetic mice. FP15 treatment reduced tyrosine nitration in the diabetic pancreatic islets. CONCLUSIONS: The current results demonstrate the importance of endogenous peroxynitrite generation in the pathogenesis of autoimmune diabetes and diabetic cardiovascular complications. Peroxynitrite decomposition catalysts may be of therapeutic utility in diabetes and other pathophysiologic conditions.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Molecular Medicine 8 : 10 (2002), p. 571-580. -
További szerzők:Mabley, Jon G. Moeller, Suzanne M. Shimanovich, Roman Pacher Pál Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Soriano, Francisco Garcia Van Duzer, John H. Williams, William Salzman, Andrew L. Groves, John T.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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9.

001-es BibID:BIBFORM048676
035-os BibID:PMID:23727362
Első szerző:Virág László (biokémikus, sejtbiológus, farmakológus)
Cím:50Years of poly(ADP-ribosyl)ation / László Virág
Dátum:2013
ISSN:0098-2997 1872-9452
Megjegyzések:The seminal paper published in 1963 by Chambon, Weil and Mandel reporting a new NAD-dependent protein modification now known as poly(ADP-ribosyl)ation (PARylation) marked the launch of a new era in both protein research and cell biology. In the coming decades, the identity, biochemical characteristics and regulation of enzymes responsible for the synthesis and degradation of protein-bound poly(ADP-ribose) have been discovered and the surprisingly multifarious biological roles of PARylation have not ceased to amaze cell and molecular biologists ever since. The review series on PARylation following this preface is comprised of ten papers written by great experts of the field and aims to provide practicing physicians and basic scientists with the state-of-the-art on the "writers, readers and erasers" of poly(ADP-ribose), some recent paradigm shifts of the field and its translational potential.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Carcinogenesis
Cell death
PARG
PARP
Poly(ADP-ribose)
Poly(ADP-ribose) polymerase
Transcription
Molekuláris Medicina
Megjelenés:Molecular Aspects of Medicine. - 34 : 6 (2013), p. 1043-1045. -
Pályázati támogatás:TÁMOP-4.2.2-08/1-2008-0019
TÁMOP
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Oxidatív stressz és ADP-riboziláció kapcsolatának vizsgálata
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Intézményi repozitóriumban (DEA) tárolt változat
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10.

001-es BibID:BIBFORM048677
035-os BibID:PMID:23416893
Első szerző:Virág László (biokémikus, sejtbiológus, farmakológus)
Cím:Poly(ADP-ribose) signaling in cell death / László Virág, Agnieszka Robaszkiewicz, Jose Manuel Rodriguez-Vargas, Francisco Javier Oliver
Dátum:2013
ISSN:0098-2997 1872-9452
Megjegyzések:Poly(ADP-ribosyl)ation (PARylation) is a reversible protein modification carried out by the concerted actions of poly(ADP-ribose) polymerase (PARP) enzymes and poly(ADP-ribose) (PAR) decomposing enzymes such as PAR glycohydrolase (PARG) and ADP-ribosyl hydrolase 3 (ARH3). Reversible PARylation is a pleiotropic regulator of various cellular functions but uncontrolled PARP activation may also lead to cell death. The cellular demise pathway mediated by PARylation in oxidatively stressed cells has been described almost thirty years ago. However, the underlying molecular mechanisms have only begun to emerge relatively recently. PARylation has been implicated in necroptosis, autophagic cell death but its role in extrinsic and intrinsic apoptosis appears to be less predominant and depends largely on the cellular model used. Currently, three major pathways have been made responsible for PARP-mediated necroptotic cell death: (1) compromised cellular energetics mainly due to depletion of NAD, the substrate of PARPs; (2) PAR mediated translocation of apoptosis inducing factor (AIF) from mitochondria to nucleus (parthanatos) and (3) a mostly elusive crosstalk between PARylation and cell death/survival kinases and phosphatases. Here we review how these PARP-mediated necroptotic pathways are intertwined, how PARylation may contribute to extrinsic and intrinsic apoptosis and discuss recent developments on the role of PARylation in autophagy and autophagic cell death.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Apoptosis
Autophagy
Cell death
Necroptosis
Necrosis
Oxidative stress
Poly(ADP-ribose) glycohydrolase
Poly(ADP-ribose) polymerase
Molekuláris Medicina
Megjelenés:Molecular Aspects of Medicine. - 34 : 6 (2013), p. 1153-1167. -
További szerzők:Robaszkiewicz, Agnieszka (1983-) (biokémikus) Rodriguez-Vargas, Jose Manuel Oliver, Francisco Javier
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0025
TÁMOP
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Oxidatív stressz és ADP-riboziláció kapcsolatának vizsgálata
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Intézményi repozitóriumban (DEA) tárolt változat
Borító:

11.

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
Borító:

12.

001-es BibID:BIBFORM028438
Első szerző:Zingarelli, Basilia
Cím:Oxidation, tyrosine nitration and cytostasis induction in the absence of inducible nitric oxide synthase / Zingarelli B., Virág L., Szabó A., Cuzzocrea S., Salzman A. L., Szabó Cs.
Dátum:1998
ISSN:1107-3756
Megjegyzések:In the present study, we evaluated the impact of the lack of the gene for inducible nitric oxide synthase (iNOS) on oxidation, tyrosine nitration and cytotoxicity reactions triggered by immunostimulation. In mice injected with E. coli endotoxin (bacterial lipopolysaccharide, LPS, 50 mg/kg i.p.), there was a significant increase in the degree of oxidation of dihydrorhodamine 123 to rhodamine 123. This response was attenuated by inhibition of NO biosynthesis with NG-methyl-L-arginine (L-NMA, 30 mg/kg i.p.). In mice lacking functional iNOS gene (iNOS knock-out mice), the degree of the LPS-induced, L-NMA inhibitable increase in dihydrorhodamine oxidation was decreased, but not completely abolished. LPS stimulation induced a marked increase in the immunoreactivity for nitrotyrosine (an indicator of peroxynitrite formation), as measured in the aorta and lung. An L-NMA inhibitable increase in nitrotyrosine staining induced by LPS was also observed in the tissues of the iNOS knockout animals. LPS treatment induced the appearance of DNA single strand breakage and a suppression of mitochondrial respiration in peritoneal macrophages ex vivo. A significant degree of LPS-induced DNA single strand breakage and suppression of mitochondrial respiration was still observed in the peritoneal macrophages obtained from the iNOS knockout animals. Macrophages from wild-type mice stimulated with LPS and interferon-gamma suppressed the proliferation of various target cells (P815 mastocytoma, L929 fibrosarcoma and embryonic lung fibroblast cell line): this effect was abolished by in vitro treatment with L-NMA (1 mM). Macrophages from the iNOS knockout animals exhibited a reduced degree of target cell cytostatic activity. The remainder of the cytostasis in iNOS knockout macrophages was abolished by preventing cell contact and neutralizing tumor necrosis factor á. The present results demonstrate that the lack of iNOS gene does not fully abolish oxidation, tyrosine nitration and cytostatic activity in response to immunostimulation. The current findings may have implications for the development of NO-based approaches for the experimental therapy of inflammation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:International Journal Of Molecular Medicine 1 : 5 (1998), p. 787-795. -
További szerzők:Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Szabó A. Cuzzocrea, Salvatore Salzman, Andrew L. Szabó Csaba (1967-) (orvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
Borító:
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