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001-es BibID:BIBFORM041943
Első szerző:Bak István (vegyész, analitikus, farmakológus)
Cím:Heme oxygenase-1 related carbon monoxide production and ventricular fibrillation in isolated ischemic/reperfused mouse myocardium / Istvan Bak, Levente Szendrei, Tibor Turoczi, Gabor Papp, Ferenc Joo, Dipak K. Das, Joel de Leiris, Peter Der, Bela Juhasz, Edit Varga, Ildiko Bacskay, Jozsef Balla, Peter Kovacs, Arpad Tosaki
Dátum:2003
ISSN:0892-6638
Megjegyzések:Heme oxygenase-1 (HO-1)-dependent carbon monoxide (CO) production related to reperfusion-induced ventricular fibrillation (VF) was studied in HO-1 wild-type (+/+), heterozygous (+/-), and homozygous (-/-) isolated ischemic/reperfused mouse heart. In HO-1 homozygous myocardium, under aerobic conditions, HO-1 enzyme activity, HO-1 mRNA, and protein expression were not detected in comparison with aerobically perfused wild-type and heterozygous myocardium. In wild-type, HO-1 hetero- and homozygous hearts subjected to 20 min ischemia followed by 2 h of reperfusion, the expression of HO-1 mRNA, protein, and HO-1 enzyme activity was detected in various degrees. A reduction in the expression of HO-1 mRNA, protein, and enzyme activity in fibrillated wild-type and heterozygous myocardium was observed. In reperfused/nonfibrillated wild-type and heterozygous hearts, a reduction in HO-1 mRNA, protein expression, and HO-1 enzyme activity was not observed, indicating that changes in HO-1 mRNA, protein, and enzyme activity could be related to the development of VF. These changes were reflected in the HO-1-related endogenous CO production measured by gas chromatography. In HO-1 knockout ischemic/reperfused myocardium, all hearts showed VF, and no detection in HO-1 mRNA, protein, and enzyme activity was observed. Thus, interventions that are able to increase endogenous CO may prevent the development of VF.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Faseb Journal 17 : 14 (2003), p. 2133-2135. -
További szerzők:Szendrei Levente Turóczi Tibor (1976-) (molekuláris biológus) Papp Gábor (farmakológus) Joó Ferenc (1949-) (vegyész) Das, Dipak Kumar de Leiris, Joel Dér Péter Juhász Béla (1978-) (kísérletes farmakológus) Varga Edit (gyógyszerész) Bácskay Ildikó (1969-) (gyógyszerész, gyógyszertechnológus) Balla József (1959-) (belgyógyász, nephrológus) Kovács Péter (1939-) (farmakológus) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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2.

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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3.

001-es BibID:BIBFORM031969
Első szerző:Szendrei Levente
Cím:Mitochondrial gene expression and ventricular fibrillation in ischemic/reperfused nondiabetic and diabetic myocardium / Szendrei L., Turoczi T., Kovacs P., Vecsernyes M., Das D. K., Tosaki A.
Dátum:2002
Megjegyzések:We investigated the mitochondrial gene expression related to cardiac function and ventricular fibrillation (VF) in ischemic/reperfused nondiabetic and diabetic myocardium. To identify potentially more specific gene responses we performed subtractive screening, Northern blotting, and reverse transcription-polymerase chain reaction (RT-PCR) of mitochondrial genes expressed after 30 min ischemia followed by 120 min reperfusion in isolated rat hearts that showed VF or did not show VF. Cytochrome oxidase B subunit III (COXBIII) and ATP synthase subunit 6, studied and selected out of 40 mitochondrial genes by subtractive screening, showed an expression after 30 min ischemia (no VF was recorded) in both nondiabetic and diabetic subjects. Upon reperfusion, the down-regulation of these genes was only observed in fibrillated hearts. Such a reduction in signal intensity was not seen in nonfibrillated myocardium. In additional studies, nondiabetic and diabetic hearts, without the ischemia/reperfusion protocol, were subjected to electrical fibrillation, and a significant reduction in COXBIII and ATPS6 mRNA signal intensity was observed indicating that VF contributes to the down-regulation of these genes. Cardiac function (heart rate, coronary flow, aortic flow, left ventricular developed pressure) showed no correlation between the up- and down-regulation of these mitochondrial genes in both nondiabetic and diabetic ischemic/reperfused myocardium. Our data suggest that COXBIII and ATPS6 may play a critical role in arrhythmogenesis, and the stimulation of COXBIII and ATPS6 mRNA expression may prevent the development of VF in both nondiabetic and diabetic ischemic/reperfused myocardium
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Biochemical Pharmacology. - 63 : 3 (2002), p. 543-552. -
További szerzők:Turóczi Tibor (1976-) (molekuláris biológus) Kovács Péter (1939-) (farmakológus) Vecsernyés Miklós (1959-) (gyógyszertechnológus, endokrinológus) Das, Dipak Kumar Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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