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001-es BibID:	BIBFORM027559
Első szerző:	Bak István (vegyész, analitikus, farmakológus)
Cím:	The role of heme oxygenase-related carbon monoxide and ventricular fibrillation in ischemic/reperfused hearts / Istvan Bak, Gabor Papp, Tibor Turoczi, Edit Varga, Levente Szendrei, Miklos Vecsernyes, Ferenc Joo, Arpad Tosaki
Dátum:	2002
Megjegyzések:	Reperfusion-induced ventricular fibrillation (VF) and heme oxygenase (HO)-related carbon monoxide (CO) production in isolated ischemic/reperfused rat hearts were studied by gas chromatography. Hearts were subjected to 30 min ischemia followed by 2 h reperfusion, and the expression of HO-1 mRNA (about 4-fold) was observed in ischemic/reperfused-nonfibrillated hearts. In fibrillated hearts, the reduction (about 75%) in HO-1 mRNA expression was detected. These changes in HO-1 mRNA expression were reflected in tissue CO production. Thus, in the absence of VF, CO production was increased about 3.5-fold, while in the presence of VF, CO production was under the detectable level in comparison with the control group. Our results suggest that the stimulation of HO-1 mRNA expression may lead to the prevention of reperfusion VF via an increase in endogenous CO production. To prove this, hearts were treated with 1 microM of N-tert-butyl-alpha-phenylnitrone (PBN) as an inducer of HO-1. PBN treatment resulted in about 20 times increase in HO-1 mRNA expression, and even a higher production rate in endogenous CO. HO protein level and enzyme activity followed the same pattern, as it was observed in HO-1 mRNA expression, in fibrillated and nonfibrillated myocardium. Five mM/l of zinc-protoporphyrin IX (ZnPPIX) significantly blocked HO enzyme activity and increased the incidence of VF, therefore the application of ZnPPIX led to a significant reduction in HO-1 mRNA and protein expression. Our data provide direct evidence of an inverse relationship between the development of reperfusion-induced VF and endogenous CO production. Thus, interventions that are able to increase tissue CO content may prevent the development of reperfusion-induced VF.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Free Radical Biology & Medicine. - 33 : 5 (2002), p. 639-648. -
További szerzők:	Papp Gábor (1976-) (vegyész, kémikus) Turóczi Tibor (1976-) (molekuláris biológus) Varga Edit (gyógyszerész) Szendrei Levente Vecsernyés Miklós (1959-) (gyógyszertechnológus, endokrinológus) Joó Ferenc (1949-) (vegyész) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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001-es BibID:	BIBFORM013594
Első szerző:	Bakondi Edina (biokémikus, vegyész)
Cím:	Age-related loss of stress-induced nuclear proteasome activation is due to low PARP-1 activity / Bakondi Edina, Catalgol Betul, Bak Istvan, Jung Tobias, Bozaykut Perinur, Bayramicli Mehmet, Ozer Nesrin Kartal, Grune Tilman
Dátum:	2011
ISSN:	0891-5849
Megjegyzések:	Changes in protein turnover are among the dominant metabolic changes during aging. Of special importance is the maintenance of nuclear protein homeostasis to ensure a coordinated cellular metabolism. Therefore, in the nucleus a special PARP-1-mediated mechanism of proteasomal activation exists to ensure a rapid degradation of oxidized nuclear proteins. It was already demonstrated earlier that the cytosolic proteasomal system declines dramatically with aging, whereas the nuclear proteasome remains less affected. We demonstrate here that the stress-mediated proteasomal activation in the nucleus declines during replicative senescence of human fibroblasts. Furthermore, we clearly show that this decline in the PARP-1-mediated proteasomal activation is due to a decline in the expression and activity of PARP-1 in senescent fibroblasts. In a final study we show that this process also happens in vivo, because the protein expression level of PARP-1 is significantly lower in the skin of aged donors compared to that of young ones. Therefore, we conclude that the rate-limiting factor in poly(ADP-ribose)-mediated proteasomal activation in oxidative stress is PARP-1 and not the nuclear proteasome itself.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban protein oxidation aging proteasome PARP nucleus free radicals külföldön készült közlemény
Megjelenés:	Free Radical Biology And Medicine. - 50 : 1 (2011), p. 86-92. -
További szerzők:	Catalgol, Betul Bak István (1975-) (vegyész, analitikus, farmakológus) Jung, Tobias Bozaykut, Perinur Bayramicli, Mehmet Ozer, Nesrin Kartal Grune, Tilman
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