We previously found that lung-specific DNA damage induced by administration of dimethylarsinic acid (DMAA), a main metabolite of inorganic arsenics in mammals, in mice might be due to dimethylarsenic peroxyl radical [(CH3)2AsOO.] produced in the further metabolic processing of DMAA. Further analysis of DNA damage was performed in the present study using a human embryonic cell line of alveolar epithelial (L-132) cells. Alkali-labile sites in DNA were produced prior to DNA single-strand breaks (SSB) and DNA-protein crosslinks (PC) in L-132 cells by exposure to 10mM DMAA. An experiment using methoxyamine (MA), an agent reacting with the aldehyde group of apurinic/apyrimidinic (AP) sites in DNA, indicated that, of the alkali-labile sites formed by exposure to DMAA, major ones were AP sites. These findings suggest that SSB and PC induced by exposure of L-132 cells to DMAA occurred via the formation of AP sites in DNA. That is, SSB were produced by a beta-elimination reaction on AP sites in the DNA and PC by a Schiff-base reaction between amino groups of nuclear proteins and aldehyde groups of AP sites.