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In this issue

ARSENITE AND PARP-1 Arsenic exposure has been known since antiquity to have a variety of adverse health effects in humans. These include liver injury, neurotoxicity, peripheral vascular disease and increased cancer risk. This is problematic because there are relatively high levels of arsenic in the drinking water in many developed areas of the world. Arsenic compounds are not mutagenic in bacterial test systems; thus, the mechanism underlying their carcinogenic properties has remained unclear. On pages 1– 6 of this issue, Hartwig et al. begin to unravel this mechanism by demonstrating that arsenite can inhibit poly(ADP-ribose) polymerase-1 (PARP-1), and that this inhibition occurs at the low, noncytotoxic concentration of 10 nM in cultured HeLa cells. PARP-1 is an important enzyme in the base-excision repair pathway; upon stimulation by DNA single or double strand breaks, it post-translationally modifies the histone proteins so that the damaged DNA dissociates from them and can then be more easily accessed by other enzymes in the DNA repair pathway. Thus, even very low levels of arsenite may increase cancer risk by interfering with DNA repair and thus contributing to genomic instability.