gene damage in cultured human alveolar ( l-132 ) cells induced by exposure to dimethylarsinic acid ( dmaa ) , a major metabolite of inorganic arsenics in mammals , was studied . 
 dna single - strand breaks and dna - protein cross - links were induced by the treatment of l-132 cells with 10 mm dmaa . 
 these kinds of damage appeared at 8 hr after start of exposure to dmaa . as regards dna - protein cross - links , the dna was found to bind not only to core histone proteins but also linker histone ( h1 ) and nonhistone proteins . 
 furthermore , the cross - links were formed by the binding to serine or threonine residues of h1 or nonhistone proteins through phosphate moieties of the dna . 
 the induction of the alkali - labile sites in dna in dmaa - treated l-132 cells was observed prior to that of dna single - strand breaks and dna - protein cross - links . 
 as one of the alkali - labile sites in dna , we estimated apurinic / apyrimidinic ( ap ) sites in dna . 
 the present study suggests that the dna single - strand breaks and dna - protein cross - links induced by the treatment of l-132 cells with dmaa occurred via the formation of ap sites in the dna and that the dna - protein cross - links were produced by a schiff - base reaction between amino groups of nuclear proteins and aldehyde groups of ap sites in the dna and the dna single - strand breaks , by a beta - elimination reaction on ap sites in the dna.imagesfigure 3 .