Apurinic/apyrimidinic (AP) sites in DNA arise via spontaneous or mutagen-induced hydrolysis of the N-glycosylic bond, or through the repair activity of DNA glycosylases (10) . If left unrepaired, AP sites are potentially lethal or mutagenic (11). To cope with the deleterious consequences of AP sites, organisms possess AP endonucleases that initiate the repair of these DNA lesions (10) . Class II AP endonucleases initiate repair by catalyzing the hydrolysis of the 5 0 -phosphodiester of an abasic site to generate a 3 0 -OH group and a 5 0 -abasic phosphate residue (10) . The substrate specificity of human apurinic endonuclease on synthetic substrate analogs has been reported previously (12) .