Congshan Li, May 2017, 3402 Bioinformatics Group

Association between sunlight exposure and melanoma has been well established in humans. However, there remains controversy on the mechanism of melanoma induction. Evidence has been reported showing both direct DNA damage by UVB and indirect cellular damage from oxidative radical production by photosensitizers (e.g., melanin) may be involved in triggering melanoma induction. Among the many documented Xiphophorus interspecies hybrid melanoma tumor models are a few known to exhibit melanoma induction only after exposure to UVB. Tumor induction studies using the UVB-inducible Xiphophorus hybrid tumor models have shown that post-UVB exposure to fluorescent light greatly diminishes or completely negates melanoma induction. This loss of UVB tumorigenic effect by exposure to FL is widely considered to be due to rapid repair of UVB-induced DNA damage by lesion specific DNA photolyases that are active in fish skin.

UV radiation is composed of UVA (320–400nM), UVB (290–320nM) and UVC (200– 290nM). Although UVC is highly mutagenic, it is completely absorbed by atmospheric ozone and does not reach the earth surface. Both UVA and UVB are genotoxic. While UVB is considered a direct cause of mutation due to DNA damage, UVA may produce genotoxicity through indirect mechanisms involving production of reactive oxygen species (ROS).

In most studies to date the biology and molecular genetic capabilities of the organism being used to model tumor induction have not been as deeply addressed as have the photochemical properties of the light source being applied to induce tumors. Accordingly, Lu et al. have initiated systematic studies of skin from parental Xiphophorus strains utilized in crosses that produce melanoma susceptible experimental genotypes after exposure to various light types and sources.

Over the past decade physiological and psychological effects of artificial fluorescent lighting on humans have been shown to be significant and quantifiable. Both the amount of light and composition of lighting are important parameters associated with human health. Differences in the inflammatory response to specific light wavelengths have been shown between human males and females. Other published reports suggest human physiological response to full spectrum vs. “cool white” lamps include differences in oxygen intake, heart rate, absorption of vitamins and minerals, etc. However, despite behavioral and physiological studies indicating artificial light sources are important to animal health, there exists a paucity of data regarding specific molecular genetic responses that occur in the intact animal upon exposure to varying types of artificial lighting.

Xiphophorus are expected to be both very sensitive and responsive to varying light conditions. In the wild, fishes must utilize light conditions for warmth, predation, predator avoidance, and to coordinate breeding cycles. Given the increasing set of genomic tools currently available, Xiphophorus represent a tractable vertebrate model to investigate the molecular genetic responses to light composition and varied light wavelengths.

Walter et al. reported that fluorescent light exposures incite a transcriptional response nearly as great in amplitude as that observed after UVB exposure and is consistent with suppression of cell cycle progression as has been observed upon entry into the light phase of the circadian cycle. Although a set of genes in fish skin is similarly affected by both UVB and fluorescent light exposure, only fluorescent light serves to down-regulate expression of genes in critical pathways expected to curtail mitotic progression.

Chang et al. reported that when Xiphophorus fish skin was exposed to six specific 50 nm wavelength regions between 300 and 600 nm, two 50 nm wavelength regions of light exhibit substantially higher levels of transcriptional response (300–350 nm and 500–550 nm) than any of the other 50 nm wavelength regions tested. Light exposure in these two wavelength regions appears to induce circadian and cellular stress responses as well as activation of p53 and other cellular processes.

 

References:

1. Boswell, W., Boswell, M., Titus, J., Savage, M., Lu, Y., Shen, J., Walter, R.B., 2015. Sex-specific molecular genetic response to UVB exposure in Xiphophorus maculatus skin. Comparative biochemistry and physiology. Toxicology & pharmacology : CBP 178, 76-85.
2. Chang, J., Lu, Y., Boswell, W.T., Boswell, M., Caballero, K.L., Walter, R.B., 2015. Molecular genetic response to varied wavelengths of light in Xiphophorus maculatus skin. Comparative biochemistry and physiology. Toxicology & pharmacology : CBP 178, 104-115.
3. Lu, Y., Bowswell, M., Bowswell, W., Yang, K., Schartl, M., Walter, R.B., 2015. Molecular genetic response of Xiphophorus maculatus-X. couchianus interspecies hybrid skin to UVB exposure. Comparative biochemistry and physiology. Toxicology & pharmacology : CBP 178, 86-92.
4. Walter, R.B., Walter, D.J., Boswell, W.T., Caballero, K.L., Boswell, M., Lu, Y., Chang, J., Savage, M.G., 2015. Exposure to fluorescent light triggers down regulation of genes involved with mitotic progression in Xiphophorus skin. Comparative biochemistry and physiology. Toxicology & pharmacology : CBP 178, 93-103.