Ionizing- and ultraviolet radiation provoke cell damage or death in a sequel that begins with DNA damage followed by NAD consumption. Several investigators have shown that interruption of the Embden-Meyerhof pathway and the depletion of cellular ATP occur subsequently. Poly(ADP)-ribose polymerase (PARP-1) is the enzyme responsible for much of the NAD degradation following DNA damage, although numerous other PARPs have been discovered recently that await functional characterization. Studies on mouse epidermis in vivo and on human cells in culture have shown that UV-B radiation provokes the transient degradation of NAD and the synthesis of ADP-ribose polymers by PARP-1. This enzyme functions as a component of a DNA damage surveillance network in eukaryotic cells to determine the fate of cells following genotoxic stress. Additionally, the activation of PARP-1 results in the activation of a nuclear proteosome that degrades damaged nuclear proteins including histones. Identifying ways to optimize the function of PARPs is likely to be very important in minimizing the deleterious effects of solar radiation on skin.