Oxidative DNA base damage produced primarily by reactive oxygen species is assumed to be the most important endogenous damage. Lack of its repair may contribute to mutagenesis, carcinogenesis and aging. It is supposed that most oxidative DNA base damage is removed by the base excision repair pathway; although it was shown recently that other DNA repair pathways could be involved. This review is focused on the role of nucleotide excision repair (NER) and transcription-coupled repair (TCR) in the removal of oxidative DNA base damage in mammalian cells.