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001-es BibID:BIBFORM028393
Első szerző:Scott, Gwen S.
Cím:Role of poly(ADP-ribose) synthetase activation in the development of experimental allergic encephalomyelitis / G. S. Scott, P. Hake, R. B. Kean, L. Virág, Cs. Szabó, D. C. Hooper
Dátum:2001
ISSN:0165-5728
Megjegyzések:Peroxynitrite formation has been demonstrated during experimental allergic encephalomyelitis (EAE). Furthermore, peroxynitrite has been identified as an activator of poly(ADP-ribose) synthetase (PARS), an enzyme implicated in neurotoxicity. In the current study, we examined the role of PARS activation in the development of EAE. Administration of the PARS inhibitor 5-iodo-6-amino-1,2-benzopyrone (INH2BP) delayed the onset of EAE and reduced the incidence and severity of disease signs. Moreover, drug treatment lowered iNOS activity and decreased cell infiltration in cervical spinal tissues from EAE-sensitized animals. To conclude, the results of the present investigation suggest that PARS activity may contribute to the pathogenesis of EAE.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
experimental allergic encephalomyelitis
poly(ADP-ribose) synthase
peroxynitrite
inflammation
blood-brain barrier
külföldön készült közlemény
Megjelenés:Journal of Neuroimmunology 117 : 1-2 (2001), p. 78-86. -
További szerzők:Hake, Paul Kean, R. B. Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Szabó Csaba (1967-) (orvos) Hooper, D. Craig
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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2.

001-es BibID:BIBFORM028374
Első szerző:Scott, Gwen S.
Cím:Peroxynitrite-induced oligodendrocyte toxicity is not dependent on poly(ADP-ribose) polymerase activation / Gwen S. Scott, Laszlo Virág, Csaba Szabó, D. Craig Hooper
Dátum:2003
ISSN:0894-1491
Megjegyzések:Oligodendrocyte loss is a characteristic feature of several CNS disorders, including multiple sclerosis (MS) and spinal cord injury. However, the mechanisms responsible for oligodendrocyte destruction remain undefined. As recent studies have implicated peroxynitrite in the pathogenesis of both spinal cord injury and MS, we have examined whether peroxynitrite may mediate at least some of the oligodendrocyte damage and demyelination observed in these conditions. Primary rat oligodendrocytes were exposed to authentic peroxynitrite in vitro and assessed for cytotoxicity. Mitochondrial function, measured by the reduction of MTT to formazan, and mitochondrial membrane potential were used as indicators of cell viability. Cell death was quantitated by measuring either the release of lactate dehydrogenase from, or the uptake of propidium iodide into, damaged and dying cells. Peroxynitrite dose-dependently reduced the viability of primary oligodendrocytes and induced cell death. Furthermore, peroxynitrite significantly increased DNA strand breakage and the activity of poly(ADP-ribose) polymerase (PARP) in oligodendrocyte cultures. To identify whether PARP activation plays a role in peroxynitrite-induced oligodendrocyte toxicity, we examined the effects of the PARP inhibitors 3-aminobenzamide (3AB) and 5-iodo-6-amino-1,2-benzopyrone (INH(2)BP) on mitochondrial function and cell death in oligodendrocytes. The presence of 3AB and INH(2)BP did not protect oligodendrocytes from peroxynitrite-induced cytotoxicity. However, both compounds significantly reduced PARP activity in these cells. Primary oligodendrocytes generated from PARP-deficient mice were also highly susceptible to peroxynitrite-induced cell death. Therefore, our results show that peroxynitrite exerts cytotoxic effects on oligodendrocytes in vitro independently of PARP activation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
free radicals
necrosis
demyelination
multiple sclerosis
spinal cord injury
egyetemen (Magyarországon) készült közlemény
Megjelenés:Glia 41 : 2 (2003), p. 105-116. -
További szerzők:Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Szabó Csaba (1967-) (orvos) Hooper, D. Craig
Internet cím:Szerző által megadott URL
DOI
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