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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:	BIBFORM030562
Első szerző:	Pázmándi Kitti Linda (molekuláris biológus, immunológus)
Cím:	Modulatory effects of low-dose hydrogen peroxide on the function of human plasmacytoid dendritic cells / Kitti Pazmandi, Zoltan Magyarics, Istvan Boldogh, Aniko Csillag, Eva Rajnavolgyi, Attila Bacsi
Dátum:	2012
ISSN:	0891-5849
Megjegyzések:	Under normal conditions, plasmacytoid dendritic cells (pDCs) are located in peripheral lymphoid organs or circulate in the blood, from where they can migrate to sites of infection or inflammation. In inflamed tissues, pDCs can be exposed to elevated levels of reactive oxygen species produced by inflammatory cells and we presume that oxidative stress could affect the cellular responses of pDCs to microenvironmental stimuli. To explore this possibility, human pDCs isolated from peripheral blood of healthy donors were treated with H(2)O(2) and R837 (a Toll-like receptor 7 ligand), separately and in combination. Our results demonstrate that treatment with a low concentration (0.01?M) of H(2)O(2) resulted in only slight changes in the expression of CD40, CD80, CD86, and CD83; however, low-dose H(2)O(2) markedly decreased the expression of HLA-DQ on pDCs. Exposure to H(2)O(2) did not trigger the release of IL-6, TNF-?, IL-8, or IFN-? from pDCs. Although addition of H(2)O(2) did not modify the capacity of pDCs to activate allogeneic IL-17- or IFN-?-producing T cells, it significantly increased the ability of pDCs to stimulate IL-4-secreting T cells. Exposure of pDCs to H(2)O(2) before cocultivation with naïve autologous T cells significantly lowered IL-10 production by T cells, but did not affect IL-17 release. It was also observed that H(2)O(2)-exposed pDCs provided stronger stimuli for Th2 than for Th1 differentiation upon autologous activation, compared to untreated pDCs, possibly because of elevated surface expression of OX40-L. Most importantly, when pDCs were stimulated with R837 in the presence of H(2)O(2), decreased phenotypic activation, decreased chemokine and cytokine release, and impaired allo- and autostimulatory functions of pDCs were detected, indicating that pDCs exposed to oxidative stress in vivo may have an anti-inflammatory or tolerogenic role in regulating adaptive immune responses.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Molekuláris Medicina Plasmacytoid dendritic cells Oxidative stress Inflammation Immune regulation Free radicals egyetemen (Magyarországon) készült közlemény
Megjelenés:	Free Radical Biology and Medicine 52 : 3 (2012), p. 635-645. -
További szerzők:	Magyarics Zoltán (1982-) (immunológus) Boldogh István Csillag Anikó (1979-) (immunológus, biológus, angol-magyar szakfordító) Rajnavölgyi Éva (1950-) (immunológus) Bácsi Attila (1967-) (immunológus)
Pályázati támogatás:	TÁMOP-4.2.1/B-09/1/KONV-2010-0007 TÁMOP Molekuláris immunológia
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