Elektron transzfer rendszerek élettani szerepe = The physiological role of electron transfer systems

Fagocitakban leirtuk a NADPH oxidazt szabalyozo ket kulonboző GTPaz aktivalo feherje szabalyozasat es a kiserő K+ transzport bakterium olő hatasat. Agyi mitokondriumokban (mito) a legzesi lanc I. komplexenek szubsztratjai membranpotencial (Em) fuggően reaktiv oxigenszarmazekot (ROS) kepeznek. Az alfa-glicerofoszfat (aGP) ROS-t kepez az I. komplexen es az aGP-dehidrogenaz enzimen, utobbit a Ca2+ aktivaja. Idegvegződesekben a mito ROS kepzeset az Em nem befolyasolja. A mito-k elektromos szinciciumot kepeznek, de a Ca2+ diffuzioja korlatozott. Alacsony O2.- szint a Ca2+ -mobilizalo agonista Ca2+ jel kepző hatasat glomeruloza sejtben gatolja. A ROS tamadaspontja a belső raktarbol tortenő Ca2+ felszabadulas. UV hatasara a mito Ca2+ felvetele is csokkent. Angiotenzin II -vel ingerelt H295R sejtben a mito Ca2+ jel kepzes sebessege a mito es az endoplazmas retikulum (ER) kozelsegevel korrelal. A p38 MAPK es az ujtipusu PKC izoformak egyidejű gatlasa a Ca2+ jelnek a citoszolbol a mito-ba tortenő attevődeset gatolja es a fenti korrelaciot megszunteti. Az ER lumeneben a tiol/diszulfid rendszertől elkulonulő NAD(P)+/NAD(P)H rendszer műkodik. Redox allapotat a glukoz-6-foszfat transzporter es az intraluminalis oxidoreduktazok hatarozzak meg. A redukalt allapot fenntartasa szukseges a glukokortikoidok prereceptorialis aktivalasahoz, s egyes sejtekben antiapoptotikus hatasu. Jellemeztuk az ER szulfat transzporteret, valamint a transzlokon peptid csatorna anion permeabilitasat. | We described in phagocytes the regulation of two GTPase activating proteins, terminating the activity of plasmalemmal NADPH oxidase and the role of K+ movements in bacterial killing. In brain mitochondria complex I dependent substrates show a membrane potential (Em) dependent reactive oxygen species (ROS) formation. ROS production by alpha-glycerophosphate (aGP) occured at complex I and on the aGP-dehydrogenase enzyme. The latter is activited by Ca2+. Mitochondria form an electric syntitium but the diffusion of Ca2+ is limited. In glomerulosa cells, at low [O2.-] angiotensin-induced Ca2+ signalling is attenuated, the site of ROS action is Ca2+ release from the internal stores. The rate of mitochondrial Ca2+ uptake in angiotensin-stimulated cells correlates with the vicinity of the mitochondrion and the endoplasmic reticulum (ER). Simultaneous activation of p38 MAPK and the novel isoforms of PKC attenuates the transfer of cytosolic Ca2+ signal into the mitochondria and abolishes this correlation. In the ER we observed a novel NAD(P)+/NAD(P)H system different from the thiol/disulphide system. Its reduced state is tuned by the glucose-6-phosphate transporter and the luminal oxidoreductases and is required for the prereceptorial activation of glucocorticoids. We have characterized the sulphate transport in the ER, and the contribution of the translocon peptide channel to the membrane permeation of small anions.