Oksidativni stres predstavlja disbalans u homeostazi egzogenih i endogenih oksidanasa. Prisustvo povećanih koncentracija oksidanasa u ćelijama i ekstracelularnim tečnostima dovodi do spntanih post-translacionih modifikacija proteina i utiče na njihove hemijske, biološke, fizičke i imunogene osobine, i predstavlja deo molekulskih mehanizama mnogih bolesti. Do sada su opisane brojne post-translacione modifikacije proteina u uslovima oksidativnog stresa. Pored direktnog oksidantnog dejstva kiseonikovih i azotnih slobodnih radikala, i brojni drugi oksidansi učestvuju u post-translacionim modifikacijama proteina. Tako se glikaciom i glikoksidacijom stvaraju AGE (advanced glycation end-products), reakcijom sa lipidnim aldehidima i ketonima ALE (advanced lipoxidation end-products), oksidacijom i polimerizacijom AOPP (advanced oxidation protein products), a reakcijom sa ureom i/ ili izocijanskom kiselinom nastaju produkti karabmoilacije proteina. U ovom preglednom članku dat je opis hemijskih modifikacija proteina sa posebnim osvrtom na značaj u patogenetskom mehanizmu razvoja pojedinih bolesti kod čoveka.
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