Oxidative DNA damage has been shown to accumulate with age in the nuclear and mitochondrial genome and cause cancer. Among DNA lesions produced by reactive oxygen species, base lesions and single-strand breaks are most frequently produced and cause mutation and cell death. However, these lesions are effectively repaired by base excision repair, which is very well conserved from bacteria to human. Since many proteins are involved in the repair process, understanding of their functions and the effects of repair deficiency will provide the relation between DNA damage and aging-related diseases. For this purpose we analyzed the proteins involved in the repair of oxidative DNA damage and found novel mechanisms protecting mammals against oxidative stresses.