A comprehensive investigation has been made of photoreactivation of UV damage in cells cultured from the fat-tailed marsupial mouse, Sminthopsis crassicaudata. Maximal photoreversal of the lethal effects of germicidal UV radiation was obtained by exposure of cells to intense fluorescent black light at 37 degrees C. Dose-reduction factors of approximately 2 were obtained. This phenomenon was shown to be a true photoreactive not a photoprotective effect. Attempts to photoreverse the lethal effects of UV light by using white fluorescent light, or black lights at lower temperatures, proved ineffectual. Photoreactivation with black light at 37 degrees C for 30 min effectively photoreversed UV-induced pyrimidine dimers and also substantially reduced the levels of UV-induced DNA-repair replication. Sunlight was also found to be an effective source of photoreactivating light. Although a reasonable correlation was found between the lethal effects of UV light and the number of pyrimidine dimers persisting unrepaired in cellular DNA, some experiments did suggest that either a small subclass of dimers or some type of non-dimer damage contributed significantly to overall lethality. Two of the effects induced by UV light could not, however, be reversed by black light. These were sister-chromatid exchanges and the inhibition of DNA synthesis. The conclusion was reached that either these effects reflect non-dimer (non-photoreactivable damage) or that, under appropriate growth conditions, some damage rapidly disrupts the DNA, say within a replicon, in a manner which cannot be reversed even when the primary lesion has been subsequently removed.