članak: 1 od 1  
Journal of the Serbian Chemical Society
2005, vol. 70, br. 4, str. 601-608
jezik rada: engleski
kratki članak
doi:10.2298/JSC0504601S

Mangan-superoksid-dismutaza (MnSOD) katalizuje NO-zavisno nitrovanje ostatka tirozina
aUniverzitet u Beogradu, Hemijski fakultet
bInstitut za hemiju, tehnologiju i metalurgiju - IHTM, Beograd
cCenter for Food Analysis, Belgrade
dInstitut za biološka istraživanja 'Siniša Stanković', Beograd


Projekat Ministarstva nauke Republike Srbije, br. HE1569

Sažetak

Dobro je poznato da peroksinitrit izaziva nitrovanje ostataka tirozina u mangan-superoksid- dismutazi (MnSOD) što dovodi do inaktivacije enzima. Pokazano je da nitrovanje i inaktivacija MnSOD-a nastaje u raznim bolestima za koje je karakteristič an oksidativni stres i povećana produkcija azot-monoksida (NO). Pošto se pri ovim uslovima očekuje nastajanje peroksinitrita predloženo je da peroksinitrit izaziva nitrovanje i inaktivaciju MnSOD in vivo. U našem prethodnom radu pokazali smo da MnSOD katalizuje transformaciju NO u nitrozonijum (NO+) i nitroksil (NO–) reaktivne vrste, te identifikovali neke od modifikacija molekula enzima koje pri tome nastaju izazivajući njegovu inaktivaciju. U ovom radu je pokazano da pri izlaganju MnSOD azot-monoksidu dolazi i do nitrovanja ostatka tirozina u molekulu enzima, što doprinosi njegovoj inaktivaciji. Ovi rezultati ukazuju da pri interakciji MnSOD sa NO dolazi do nastajanja nitrujućih vrsta, što baca novo svetlo na proces nitrovanja ostataka tirozina i inaktivaciju MnSOD in vivo. Ovo može da predstavlja novi mehanizam kojim MnSOD štiti ćeliju odštetnih efekata izazvanih hiperprodukcijom azot-monoksida. Međutim ekstenzivne modifikacije i inaktivacija MnSOD do kojih dolazi pri produženom izlaganju enzima NO, uvećaće toksične efekte izazvane povećanim koncentracijama superoksida i NO u ćeliji.

Ključne reči

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