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1.

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)
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2.

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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3.

001-es BibID:BIBFORM041210
035-os BibID:PMID:11033413
Első szerző:Csonka Csaba
Cím:Effects of oxidative stress on the expression of antioxidative defense enzymes in spontaneously hypertensive rat hearts / Csaba Csonka, Tunde Pataki, Peter Kovacs, Sebastian L. Müller, Matthias L. Schroeter, Arpad Tosaki, Ingolf E. Blasig
Dátum:2000
Megjegyzések:Little is known concerning the effect of oxidative stress on the expression of antioxidative enzymes in the decompensated cardiac hypertrophy of spontaneously hypertensive rats (SHR), considered as a model of dilative cardiomyopathy in man. Superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx) were characterized in isolated perfused hearts of 18 month old SHR and the age-matched normotensive control Wistar-Kyoto (WKY) rats, before and after 30 min infusion of 25 microM H(2)O(2). After infusion of H(2)O(2), aortic flow decreased in WKY from 26.2 +/- 2.2 to 16.0 +/- 0.8 ml/min (p <.05) but not in SHR (18.2 +/- 1.9 vs. 20.7 +/- 2.2 ml/min). This protection was related to the higher myocardial activities of GPx, MnSOD and CuZnSOD in SHR, compared with those of the WKY group. Although total SOD activity in the SHR fell after H(2)O(2) exposure (to 1.81 +/- 0.13 from 3.56 +/- 0.49 U/mg of protein), catalase activity increased (to 2.46 +/- 0.34 from 1.56 +/- 0.29 k min(-1)mg(-1)protein), compared with the pre-infusion period (p <.05 in each case). In additional studies, hearts were subjected to 30 min of global ischemia followed by 30 min of reperfusion. The results obtained in ischemic/reperfused hearts show the same changes in enzyme activities measured as it was observed in H(2)O(2) perfused hearts, indicating that oxidative stress is independent of the way it was induced. The higher catalase activity derived from elevated mRNA synthesis. The antioxidative system in dilative cardiomyopathic hearts of SHR is induced, probably due to episodes of oxidative stress, during the process of decompensation. This conditioning of the antioxidative potential may help overcome acute stress situations caused by reactive oxygen species in the failing myocardium.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Free Radical Biology & Medicine 29 : 7 (2000), p. 612-619. -
További szerzők:Pataki Tünde (1971-) (farmakológus, klinikai farmakológus) Kovács Péter (1939-) (farmakológus) Müller, Sebastian L. Schroeter, Matthias L. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Blasig, Ingolf E.
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4.

001-es BibID:BIBFORM011467
Első szerző:Mukherjee, Subhendu
Cím:Expression of the longevity proteins by both red and white wines and their cardioprotective components, resveratrol, tyrosol, and hydroxytyrosol / Mukherjee S., Lekli I., Gurusamy N., Bertelli A. A., Das D. K.
Dátum:2009
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Free Radical Biology and Medicine. - 46 : 5 (2009), p. 573-578. -
További szerzők:Lekli István (1981-) (gyógyszerész) Gurusamy, Narasimman Bertelli, Alberto A. A. Das, Dipak Kumar
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5.

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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6.

001-es BibID:BIBFORM002227
Első szerző:Thirunavukkarasu, Mahesh
Cím:Resveratrol alleviates cardiac dysfunction in streptozotocin-induced diabetes : role of nitric oxide, thioredoxin, and heme oxygenase / Mahesh Thirunavukkarasu, Suresh Varma Penumathsa, Srikanth Koneru, Bela Juhasz, Lijun Zhan, Hajime Otani, Debasis Bagchi, Dipak K. Das, Nilanjana Maulik
Dátum:2007
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Free Radical Biology and Medicine. - 43 : 5 (2007), p. 720-729. -
További szerzők:Penumathsa, Suresh Varma Koneru, Srikanth Juhász Béla (1978-) (kísérletes farmakológus) Zhan, Lijun Otani, Hajime Bagchi, Debasis Das, Dipak Kumar Maulik, Nilanjana
Internet cím:elektronikus változat
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7.

001-es BibID:BIBFORM002216
Első szerző:Thirunavukkarasu, Mahesh
Cím:VEGFR1 (Flt-1+/-) gene knockout leads to the disruption of VEGF-mediated signaling through the nitric oxide/heme oxygenase pathway in ischemic preconditioned myocardium / Mahesh Thirunavukkarasu, Bela Juhasz, Lijun Zhan, Venugopal P. Menon, Arpad Tosaki, Hajime Otani, Nilanjana Maulik
Dátum:2007
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Free Radical Biology and Medicine 42 : 10 (2007), p. 1487-1495. -
További szerzők:Juhász Béla (1978-) (kísérletes farmakológus) Zhan, Lijun Menon, Venugopal P. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Otani, Hajime Maulik, Nilanjana
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