Our cellular genome is continuously exposed to a wide spectrumof exogenous and endogenous DNA damaging agents. These agents canlead to formation of an extensive array of DNA lesions including single-and double-stranded breaks, inter- and intrastrand cross-links, abasicsites, and modification of DNA nucleobases. Persistence of these DNAlesions can be both mutagenic and cytotoxic, and can cause alteredgene expression and cellular apoptosis leading to aging, cancer, andvarious neurological disorders. To combat the deleterious effectsof DNA lesions, cells have a variety of DNA repair pathways responsiblefor restoring damaged DNA to its canonical form. Here we examine oneof those repair pathways, the base excision repair (BER) pathway,a highly regulated network of enzymes responsible for repair of modifiednucleobase and abasic site lesions. [ABSTRACT FROM AUTHOR]