Találati lista | Tudóstér

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
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	BIBFORM059782
035-os BibID:	(WOS)000363822600014 (Scopus)84940040945
Első szerző:	Csépányi Evelin (gyógyszerész)
Cím:	Cardiovascular effects of low versus high-dose beta-carotene in a rat model / Evelin Csepanyi, Attila Czompa, David Haines, Istvan Lekli, Edina Bakondi, Gyorgy Balla, Arpad Tosaki, Istvan Bak
Dátum:	2015
ISSN:	1043-6618
Megjegyzések:	?-carotene (BC), a lipid-soluble tetraterpene precursor to vitamin A, widely distributed in plants, including many used in human diet, has well-known health-enhancing properties, including reducing risk of and treatment for certain diseases. Nevertheless, BC may also act to promote disease through the activity of BC derivatives that form in the presence of external toxicants such as cigarette smoke and endogenously-produced reactive oxygen species. The present investigation evaluates the dose-dependent cardioprotective and possibly harmful properties of BC in a rat model. Adult male rats, were gavage-fed BC for 4 weeks, at dosages of either 0, 30 or 150 mg/kg/day. Then hearts excised from the animals were mounted in a "working heart" apparatus and subjected to 30 minutes of global ischemia, followed by 120 minutes of reperfusion. A panel of cardiac functional evaluations was conducted on each heart. Infarct size and total antioxidant capacity of the myocardium were assessed. Heart tissue content of heme oxygenase-1 (HO-1) by Western blot analysis; and potential direct cytotoxic effects of BC by MTT assay were evaluated. Hearts taken from rats receiving 30 mg/kg/day BC exhibited significantly improved heart function at lower reperfusion times, but lost this protection at higher BC dosage and longer reperfusion times. Myocardial HO-1 content was significantly elevated dose-responsively to both BC dosage. Finally, in vitro evaluation of BC on H9c2 cells showed that the agent significantly improved vitality of these cells in a dose range of 2.5-10 ?M.Although data presented here do not allow for a comprehensive mechanistic explanation for reduced cardioprotection at high dose BC, it is speculated that since Fe2+ produced as a metabolite of HO-1 activity, may determine whether BC acts as an antioxidant or prooxidant agent, the strong induction of this enzyme in response to ischemia/reperfusion-induced oxidative stress may account for the high-dose BC loss of cardioprotection.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk beta-carotene heart ischemia/reperfusion heme-oxygenase-1
Megjelenés:	Pharmacological Research. - 100 (2015), p. 148-156. -
További szerzők:	Czompa Attila (1985-) (gyógyszerész) Haines, David Donald (1981-) (gyógyszerész) Lekli István (1981-) (gyógyszerész) Bakondi Edina (1975-) (biokémikus, vegyész) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Bak István (1975-) (vegyész, analitikus, farmakológus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon:

001-es BibID:	BIBFORM014289
Első szerző:	Virág László (biokémikus, sejtbiológus, farmakológus)
Cím:	Effects of poly(ADP-ribose) polymerase inhibition on inflammatory cell migration in a murine model of asthma / Virag, L., Bai, P., Bak, I., Pacher, P., Mabley, J. G., Liaudet, L., Bakondi, E., Gergely, P., Kollai, M., Szabo, C.
Dátum:	2004
ISSN:	0891-5849 (Print)
Megjegyzések:	Poly(ADP-ribose) polymerase-1 (PARP-1), a monomeric nuclear enzyme present in eukaryotes, plays a role in cell death, inflammatory mediator expression, and mononuclear cell recruitment in various experimental models of inflammation and reperfusion injury. Part of the molecular mechanism of this function involves the regulation of cytokine and chemokine production. Since chemokines are principal regulators of mononuclear and polymorphonuclear cell trafficking in asthma, we investigated the possibility whether PARP modulates chemokine production and cell recruitment in a murine model of asthma. MATERIAL/METHODS: We studied ovalbumin-sensitized mice challenged with a single dose of ovalbumin. RESULTS: PARP inhibition with the phenanthridinone-based PARP inhibitor PJ34 suppressed inflammatory cell migration. These effects were associated with downregulation of the CC chemokine MIP-1alpha, but not the CXC chemokine MIP-2. The production of TNF- alpha and IL-12, but not IL-5 or IL-13, was also suppressed by PARP inhibition. CONCLUSIONS: Our results demonstrate the pathogenetic role of PARP activation in a murine model of asthma. PARP selectively regulates the production of certain chemokines and cytokines in this experimental model, which may be responsible for some of the observed protective effects seen in the current murine asthma model.Matrix metalloproteinase (MMP) activation contributes to the development of various pathophysiological conditions, including dilated cardiomyopathy, congestive heart failure, and reperfusion injury. Increased oxidative and nitrosative stress have been implicated in the activation of MMPs and also in the cardiotoxicity of doxorubicin (DOX), a commonly used antitumor agent. Thus, we hypothesized that MMP activation occurs in DOX-induced cardiotoxicity. Male Balb/c mice received a single injection of DOX (25 mg/kg i.p.) and were sacrificed 12 h, 1, 2, 3 and 4 days later. Hearts and aortae were harvested for MMP zymography. DOX induced time-dependent activation of MMPs both in the heart and in the aortic tissue with an earlier onset in the latter. These results demonstrate that MMP activation is an early event in DOX-induced cardiotoxicity and raises the possibility that MMP inhibitors may influence the outcome of this severe complication.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Animals Asthma/ drug therapy Bronchoalveolar Lavage Catalysis Cell Death Cell Movement Chemokine CXCL2 Chemokines/metabolism Cytokines/metabolism Disease Models, Animal Down-Regulation Enzyme Inhibitors/ pharmacology Interleukin-10/metabolism Interleukin-12/metabolism Interleukin-13/metabolism Interleukin-5/metabolism Leukocytes, Mononuclear/metabolism Lung/pathology Male Mice Mice, Inbred BALB C Ovalbumin/metabolism/pharmacology Peroxidase/metabolism Poly(ADP-ribose) Polymerases/ antagonists & inhibitors Time Factors Tumor Necrosis Factor-alpha/metabolism Antineoplastic Agents/toxicity Biological Markers/analysis Cardiomyopathy, Dilated/chemically induced/enzymology Doxorubicin/ toxicity Enzyme Activation Heart/ drug effects Heart Failure/chemically induced Matrix Metalloproteinases/ metabolism Models, Animal Myocardium/enzymology/ pathology Reperfusion Injury/chemically induced/enzymology Acute Disease Catalysis/drug effects Chronic Disease Creatine Kinase/blood Enzyme Inhibitors/pharmacology Heart/ drug effects/physiopathology Heart Failure/ chemically induced/physiopathology/prevention & control L-Lactate Dehydrogenase/blood Metalloporphyrins/ pharmacology Mice, Inbred C57BL Mice, Knockout Nitric Oxide Synthase/antagonists & inhibitors/genetics/metabolism Nitric Oxide Synthase Type II Nitric Oxide Synthase Type III Oxidative Stress/drug effects/genetics Peroxynitrous Acid/ metabolism Survival Rate Antibiotics, Antineoplastic Creatine Kinase/metabolism Doxorubicin Enzyme Activation/drug effects Heart Failure/ chemically induced/pathology/physiopathology Hemodynamics/drug effects L-Lactate Dehydrogenase/metabolism Metalloendopeptidases/metabolism Poly(ADP-ribose) Polymerases/ genetics/ metabolism Survival Analysis Ventricular Function, Left/genetics Apoptosis Benzamides/ pharmacology Caspases/metabolism Cells, Cultured DNA Damage/drug effects DNA Fragmentation/drug effects Enzyme Activation/drug effects/physiology Mitochondria/ drug effects Nitrates Nitrites/toxicity Nitrogen Oxides/ toxicity Poly(ADP-ribose) Polymerases/ antagonists & inhibitors/metabolism Protective Agents/ pharmacology Thymus Gland/cytology/ drug effects Tyrosine külföldön készült közlemény
Megjelenés:	Medical Science Monitor. - 10 : 3 (2004), p. BR77-83. -
További szerzők:	Bai Péter (1976-) (biokémikus) Bak István (1975-) (vegyész, analitikus, farmakológus) Pacher Pál Mabley, Jon G. Liaudet, Lucas Bakondi Edina (1975-) (biokémikus, vegyész) Gergely Pál (1947-) (biokémikus) Kollai, M. Szabó Csaba
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Saját polcon: