Találati lista | Tudóstér

001-es BibID:	BIBFORM040465
035-os BibID:	PMID:1308986
Első szerző:	Balla József (belgyógyász, nephrológus)
Cím:	Endothelial cell heme oxygenase and ferritin induction by heme proteins : a possible mechanism limiting shock damage / J. Balla, H. S. Jacob, Gy. Balla, K. Nath, G. M. Vercellotti
Dátum:	1992
Megjegyzések:	Acutely, hemin sensitizes endothelial cells to oxidants but chronically protects the endothelium through the induction of ferritin. By releasing its heme, methemoglobin can sensitize endothelial cells in a fashion similar to free hemin. Furthermore, prolonged incubation with the endothelium allows methemoglobin to induce heme oxygenase and ferritin and concomitantly to modulate oxidant-mediated cytotoxicity. Methemoglobin but not hemoglobin, metmyoglobin or cytochrome c induces heme oxygenase and ferritin. Heme needs to be released from methemoglobin, since sodium cyanide, haptoglobin, and hemopexin inhibit the induction of these proteins. Neutrophils can oxidize hemoglobin to methemoglobin, which can subsequently induce both heme oxygenase and ferritin. We speculate that in shock with disseminated intravascular coagulation, marginated PMNs oxidize hemoglobin to heme-releasing methemoglobin. If critical defenses such as haptoglobin and hemopexin are overwhelmed, heme enters the endothelin cells, sensitizing them to oxidant damage. Endothelial cell adaptation via heme-induced heme oxygenase and ferritin production might limit ultimate progression to pulmonary and other vascular leak syndromes.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk egyetemen (Magyarországon) készült közlemény
Megjelenés:	Transactions of the Association of American Physicians. - 105 (1992), p. 1-6. -
További szerzők:	Jacob, Harry S. Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Nath, Karl Vercellotti, Gregory M.
Borító:
Saját polcon:

001-es BibID:	BIBFORM040463
035-os BibID:	PMID:8036736
Első szerző:	Balla József (belgyógyász, nephrológus)
Cím:	Oxidized low-density lipoproteins and endothelium : oral vitamin E supplementation prevents oxidized low-density lipoprotein-mediated vascular injury / József Balla, John D. Belcher, György Balla, Harry S. Jacob, Gregory M. Vercellotti
Dátum:	1993
Megjegyzések:	Vitamin E supplements may decrease the incidence of myocardial infarction by inhibiting LDL oxidation to atherogenic moieties. We previously reported that hemin is a potent and relevant lipophilic source of iron that can rapidly intercalate into LDL, catalyzing its oxidation and promoting its cytolysis of endothelium. The effects of oral vitamin E on heme-catalyzed LDL oxidation and resulting endothelial damage were studied in 10 volunteers who received daily 800 I.U. of vitamin E with or without vitamin C (1000 mg) for 2 weeks. Prior, during, and 2 weeks after supplementation, plasma LDL was isolated and its number of alpha-tocopherol molecules, resistance to heme-catalyzed oxidation, and ability to damage porcine aortic endothelial cells were assayed. Vitamin E supplementation doubled the lag phase of LDL peroxidation as compared to control (104 +/- 18 vs. 58 +/- 11 min; p < 0.001) accompanied by an increase in alpha-tocopherol content of LDL particles (26 +/- 6 vs. 11 +/- 2 mol/mol; p < 0.001). Most intriguingly, LDL-mediated endothelial cell cytotoxicity was prevented (3 +/- 2% vs. 42 +/- 12%; p < 0.001). After a 2-week washout period, LDL alpha-tocopherol content, the lag time of LDL oxidation, and oxidized LDL-mediated cytolysis all returned to baseline levels. To determine whether supplements of vitamin E and vitamin C beneficially synergize in these effects, we monitored several volunteers on daily vitamin E alone or vitamin C alone. Vitamin E alone (at doses as low as 400 I.U./day) affected all measurements in a manner identical to that when it was taken with vitamin C. Vitamin C alone had no significant effect on these measurements. We conclude: dietary vitamin E supplementation provides cytoprotection against LDL oxidation-mediated endothelial cell injury, but this salutary effect is rapidly lost after supplementation is stopped.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban külföldön készült közlemény
Megjelenés:	Transactions of the Association of American Physicians. - 106 (1993), p. 128-133. -
További szerzők:	Belcher, John D. Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Jacob, Harry S. Vercellotti, Gregory M.
Internet cím:	Szerző által megadott URL
Borító:
Saját polcon: