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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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001-es BibID:	BIBFORM027561
Első szerző:	Pataki Tünde (farmakológus, klinikai farmakológus)
Cím:	Regulation of ventricular fibrillation by heme oxygenase in ischemic/reperfused hearts / Tunde Pataki, Istvan Bak, Csaba Csonka, Peter Kovacs, Edit Varga, Ingolf E. Blasig, Arpad Tosaki
Dátum:	2001
Megjegyzések:	We have assessed the relationship between reperfusion-induced ventricular fibrillation (VF) and heme oxygenase (HO) mRNA expression using northern blotting, reverse transcription-polymerase chain reaction (RT-PCR), and enzyme activity in isolated working ischemic/reperfused rat hearts. Isolated hearts were subjected to 30 min of global ischemia followed by 120 min of reperfusion. Upon reperfusion with VF, cardiac function was registered (n = 6 in each group), and HO mRNAs and enzyme activities were measured at the end of reperfusion in hearts that showed VF or did not develop VF. The expression of HO-1 mRNA (about fourfold) was observed in ischemic/reperfused nonfibrillated myocardium in comparison with the nonischemic control hearts. In those hearts when VF was developed, the expression of HO-1 mRNA was not observed in comparison with the nonischemic control myocardium. The results measured by RT-PCR and enzyme analysis support the data obtained by northern blotting. In additional studies, we decided to approach the question from a different angle. Thus, the purpose of our work was also to study the role of HO expression and enzyme activity in electrically fibrillated hearts without the ischemic/reperfused protocol. To simulate the period of 10 min of reperfusion-induced VF, hearts were electrically fibrillated, then defibrillated, and perfused for an additional 110 min, and HO-1 mRNA expression and enzyme activities were determined. Thus, electrically induced VF resulted in about 60%, 60%, and 70% reduction in HO-1 mRNA expression, RT-PCR signal intensity, and enzyme activity, respectively, compared with the nonfibrillated ischemic/reperfused group. In conclusion, our data provide evidence that the development of reperfusion-induced VF inhibits HO-1 mRNA expression and enzyme activity in both electrically fibrillated myocardium and ischemic/reperfused fibrillated hearts. The results clearly show that HO-1 mRNA expression and enzyme activity were increased in ischemic/reperfused nonfibrillated myocardium, suggesting that interventions that are able to increase HO-1 mRNA expression and enzyme activity may prevent the development of VF.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Antioxidants & redox signaling 3 : 1 (2001), p. 125-134. -
További szerzők:	Bak István (1975-) (vegyész, analitikus, farmakológus) Csonka Csaba Kovács Péter (1947-) (belgyógyász, kardiológus, klinikai farmakológus) Varga Edit (gyógyszerész) Blasig, Ingolf E. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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