Abstract: On a daily basis, the skin is exposed to many environmental stressors and insults. Over a 24-hr natural cycle, during the day, the skin is focused on protection; while at night, the skin is focused on repairing damage that occurred during daytime and getting ready for the next morning. Circadian rhythm provides the precise timing mechanism for engaging those different pathways necessary to keep a healthy skin through clock genes that are present in all skin cells. The strongest clue for determining cellular functions timing is through sensing light or absence of light (darkness). Here, we asked the question if blue light could be a direct entrainment signal to skin cells and also disrupt their circadian rhythm at night. Through a reporter assay for per1 transcription, we demonstrate that blue light at 410nm decreases per1 transcription in keratinocytes, showing that epidermal skin cells can sense light directly and control their own clock gene expression. This triggers cells to “think” it is daytime even at nighttime. Elsewhere, we measured different skin cell damage due to blue light exposure (at different doses and times of exposure) versus cells that were kept in full darkness. We show an increase of ROS production, DNA damage and inflammatory mediators. These deleterious effects can potentially increase overall skin damage over time and ultimately accelerates aging.

Abstract: With the exception of high latitudes, life has evolved under bright days and dark nights. Most organisms have developed endogenously driven circadian rhythms that are synchronized to this daily light/dark cycle. In recent years, humans have shifted away from the naturally occurring solar light cycle in favor of artificial and sometimes irregular light schedules produced by electric lighting. Exposure to unnatural light cycles is increasingly associated with obesity and metabolic syndrome; however, the means by which environmental lighting alters metabolism are poorly understood. Thus, we exposed mice to dim light at night and investigated changes in the circadian system and metabolism. Here we report that exposure to ecologically relevant levels of dim (5 lux) light at night altered core circadian clock rhythms in the hypothalamus at both the gene and protein level. Circadian rhythms in clock expression persisted during light at night; however, the amplitude of Per1 and Per2 rhythms was attenuated in the hypothalamus. Circadian oscillations were also altered in peripheral tissues critical for metabolic regulation. Exposure to dimly illuminated, as compared to dark, nights decreased the rhythmic expression in all but one of the core circadian clock genes assessed in the liver. Additionally, mice exposed to dim light at night attenuated Rev-Erb expression in the liver and adipose tissue. Changes in the circadian clock were associated with temporal alterations in feeding behavior and increased weight gain. These results are significant because they provide evidence that mild changes in environmental lighting can alter circadian and metabolic function. Detailed analysis of temporal changes induced by nighttime light exposure may provide insight into the onset and progression of obesity and metabolic syndrome, as well as other disorders involving sleep and circadian rhythm disruption.