Damage and repair in mammalian cells after exposure to non-ionizing radiations II. Photoreactivation and killing of rat kangaroo cells ( Potorous tridactylus) and herpes simplex virus-1 by exposure to fluorescent “white” light or sunlight

Abstract

Photoreactivation (PR) of ultraviolet (254 nm)-inactivated cornea cells of the potoroo (or rat kangaroo; Potorous tridactylus) has been studied at wavelengths > 375 nm from either fluorescent “white” light or sunlight. In both cases the PR kinetics curves pass through maxima, which most likely result from the superposition of concomitant inactivation by the photoreactivating light. The inactivating effect of light was directly demonstrated for non-UV-irradiated cells, permitting correction of the PR curves. Wavelengths > 475 nm, and even > 560 nm, which do not noticeably damage cells, still photoreactivate, though less effectively than shorter wavelengths. Light treatment of UV-resembling those observed for cells, while light treatment of unirradiated virus after infection likewise causes inactivation. The “fluence reduction factor” of PR, which is >3 for the virus, exceeds that for the cells, where it decreases with increasing UV fluence. In vitro tests have indicated that sunlight >375 nm causes photorepairable DNA lesions which are virtually fully repaired by the same light. Thus cell inactivation resulting from these solar wavelengths must be due to non-photorepairable damage.