Abstract
Genome stability is fundamental to cell viability, the evolutionary stability of organisms, and the preservation of their functional integrity. Endogenous damage, particularly the oxidative modification of nitrogenous bases resulting from cellular metabolism, is one of the main factors disrupting DNA structure. To prevent the accumulation of mutations, cells utilize a base excision repair (BER) system in which DNA glycosylases play a pivotal role. These enzymes recognize and remove damaged or mismatched bases, thereby initiating a cascade of repair reactions. Adenine DNA glycosylases belonging to the MutY/MUTYH family are unique in that they do not directly remove damaged bases, but rather correct replication errors arising from oxidative damage to guanine. In bacteria, this function is performed by the MutY enzyme, whereas in eukaryotes it is performed by its homologue, MUTYH. These enzymes prevent G:C → T:A transition mutations from becoming fixed, thereby significantly reducing the level of spontaneous mutagenesis. This review discusses the role of DNA glycosylases in maintaining genomic stability, focusing on the molecular mechanisms of adenine DNA glycosylase function, their place in the BER system, evolutionary conservation, and their significance in biotechnology, molecular genetics, and applied research.