Ultraviolet a radiation suppresses an established immune response: implications for sunscreen design.

The ultraviolet radiation present in sunlight is the primary cause of nonmelanoma skin cancer and has been implicated in the development of cutaneous malignant melanoma. In addition, ultraviolet is immune suppressive and the suppression induced by ultraviolet radiation has been identified as a risk factor for skin cancer induction. Ultraviolet also suppresses the immune response to infectious agents. In most experimental models, ultraviolet is applied to immunologically naive animals prior to immunization. Of equal concern, however, is the ability of sunlight to suppress established immune reactions, such as the recall reaction in humans, which protects against microbial infections. Here we demonstrate that solar-simulated ultraviolet radiation, applied after immunization, suppresses immunologic memory and the elicitation of delayed-type hypersensitivity. Further, we found that wavelengths in the ultraviolet A region of the solar spectrum were critical for inducing immune suppression. Ultraviolet A (320-400 nm) radiation was as effective as solar-simulated ultraviolet A + B (290-400 nm) in suppressing the elicitation of an established immune response. Irradiation with ultraviolet AI (340-400 nm) had no effect. Supporting a critical role for ultraviolet A in ultraviolet-induced immune suppression was the observation that applying a sunscreen that contained an ultraviolet B only filter had no protective effect, whereas, a sunscreen containing both ultraviolet A and ultraviolet B filters totally blocked ultraviolet-induced immune suppression. These data suggest that sunlight may depress the protective effect of prior vaccination. In addition, the observation that ultraviolet A is immunosuppressive indicates the need for ultraviolet A protection when designing sun protection strategies.

Development of a circadian melatonin rhythm in embryonic zebrafish.

We investigated the time course of circadian system development in zebrafish and the role of environmental light cycles in this process, using a rhythm in melatonin content of embryos and larvae as a marker of circadian function. When zebrafish were raised in a cycle of 14 h light and 10 h dark at 28.5 degrees C, nocturnal increases in melatonin content were detectable beginning on the second night post-fertilization (PF). When embryos were transferred to constant darkness (DD) at the end of the second light period, a circadian rhythm of melatonin content persisted for at least three cycles. However, when embryos were transferred from light to DD at 14 h PF, no rhythm was detectable in the population. Phase-locked circadian melatonin rhythms were measurable after embryos were exposed to a transition from constant light (LL) to darkness at 26 or 32 h PF, but not at 20 h. These data indicate that a circadian oscillator that regulates melatonin synthesis becomes functional and responsive by light between 20 and 26 h PF. At this stage, pineal photoreceptors have begun to differentiate, but retinal photoreceptors have not, suggesting that the first circadian melatonin rhythms are of pineal origin. The absence of melatonin rhythms in populations of embryos exposed to DD beginning at earlier stages indicates that there is no timed developmental event that sets the circadian clock in the absence of environmental input. Exposure to DD starting at 14 or 20 h PF did not retard overall development as determined by gross morphological staging criteria, and did not prevent later synchronization of melatonin rhythms by light-dark (LD) cycles.