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  • 1 Debreceni Egyetem, Orvos- és Egészségtudományi Centrum Szülészeti és Nőgyógyászati Klinika és Megelőző Orovostani Intézet Debrecen Nagyerdei krt 98. 4032
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Egészséges és praeeclampsiás terhességben a neutrophil granulocyták reaktív oxigéngyökök termeléséről szóló adatok ellentmondásosak. Céljuk volt a szuperoxid-anionnak a praeeclampsia etiológiájában betöltött szerepét tovább vizsgálni, ezért forbol-dibutiráttal és n-formil-metionil-leucil-fenilalaninnal stimulálták az egészséges nem terhesekből, egészséges terhesekből és praeeclampsiás terhesekből származó granulocytákat. Vizsgálták az említett három csoport hő által inaktivált és nem inaktivált vérplazmájának hatását a granulocyták szuperoxid-termelésére. A szuperoxid termelődését a ferricitokróm c redukciójaként mérték spektrofotometriás módszerrel. Mind a forbol-dibutirát, mind az n-formil-metionil-leucil-fenilalanin indukálta szuperoxid-termelés szignifikánsan csökkent egészséges terhesekből származó granulocyták esetében. A nem terhesekből és praeeclampsiás terhesekből származó granulocyták forbol-dibutirát stimulálta O2ˉ˙-termelődését az egészséges terhesektől nyert inaktivált és nem inaktivált vérplazma is gátolta. Az n-formil-metionil-leucil-fenilalaninnal stimulált nem terhesek és praeeclampsiás terhesek granulocytáinak O2ˉ˙-termelését csak az egészséges terhesek nem inaktivált vérplazmája tudta gátolni. Az egészséges terhesek granulocytáinak forbol-dibutirát stimulálta O2ˉ˙-termelését szignifikánsan növelte mind a nem terhesek, mind a praeeclampsiás terhesek plazmája inaktivált és nem inaktivált formában is. Az egészséges terhesek neutrophiljeinek n-formil-metionil-leucil-fenilalaninnal indukált O2ˉ˙-termelése szignifikánsan növekedett a nem terhesek és praeeclampsiások nem inaktivált plazmáinak hatására. Feltételezik, hogy az egészséges terhességben megfigyelhető csökkent O2ˉ˙-termelés anyai immunszuppresszív faktoroknak köszönhető. Ezen faktorok hiánya valószínűsíthető praeeclampsiában, így magyarázható az egészséges terhességben bekövetkező O2ˉ˙-termelődés csökkenésének elmaradása, ami a praeeclampsiában megfigyelhető endothelsejt-károsodásért is felelős lehet. Orv. Hetil., 2012, 153, 425–434.

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