UV light is present in sunlight and is also produced by electric arcs and specialized lights, such as tanning lamps, and black lights. For most terrestrial organisms, UV light (100 to 400 nm) is a common environmental toxin that must be dealt with. It is well known that exposure to UV light can lead to skin burns and fatigue. UV can increase the risk of skin cancer through damaging DNA, and the cellular response to UV exposure largely revolves around DNA damage response. For mammals, the ability to sense light is a ubiquitous and essential feature that serves a broad range of functions including synthesis of vitamin D, modulation of circadian rhythms, and informing on the environment. Previously, as a native soil organism that is not regularly exposed to UV in its natural habitat, the nematode C. elegans was believed to have the disability to sense light due to the lack of a bona fide photoreceptor system. However, recent work in C. elegans has identified the LITE-1 taste receptor, which is homolog as a UV-specific photoreceptor, and totally distinct from other photoreceptors in metazoans, microbes, and plants.
For C. elegans, exposure to UV light leads to an escape behavior (avoidance behavior) and a pharyngeal pumping inhibition (acute cessation of feeding). In contrast to animals with external pigmentation, the worms are particularly vulnerable to the mutagenic effects of UV due to the transparent body that allows the penetration of lights. Indeed, there are many UV-sensitive mutants of C. elegans. The cellular response to UV irradiation in C. elegans is homologous to the mammalian DNA damage repair pathway and includes homologs of DNA surveillance protein ataxia telangiectasia, RAD3-related kinase (ATR) and the tumor suppressor p53. It is notable that CEP-1, the C. elegans homolog of mammalian p53, plays a role in the nervous system in the behavioral response to UV light.
It is notable that when dealing with UV radiation on C. elegans in an experiment, there are a few caveats. First, the doses of UV radiation selection, which is closely related to biological questions and the UV resistance properties of the worm strains used in the assay. Second, if necessary, the response to UV radiation can be performed using different stages of worms to determine its stage-specific effects. Third, liquid can absorb UV and decreases its effective dosage, therefore liquid media culture systems are not suitable for C. elegans UV radiation stress assay. Furthermore, UV radiation can cause harmful effects in humans. Precaution should be taken when performing the assays.
UV radiation, typically as a model genotoxin, introduces bulky DNA lesions. Genes and pathways involved in DNA repair in mammals are generally well conserved in C. elegans. Previous studies pointed that nucleotide excision repair is similar between C. elegans and humans, in both conservations of genes and kinetics of repair. Therefore, we provide services to establish a cost-effective, in vivo, and genetically manipulable physiological model for the study of the toxicological consequences of DNA damage and genotoxic agents.
As a major DNA-damaging environmental stress, UV radiation induces DNA lesions and produces free radicals that damage other cellular macromolecules. Free radicals are one of the byproducts of cellular metabolism, and the most abundant free radicals in cells are reactive oxygen species (ROS), which can lead to oxidation reactions. As a key enzyme in the detoxification of free radicals, superoxide dismutase (SOD) can eliminate harmful produces during metabolism such as ROS. Therefore, we also offer services to determine the changes of ROS and SOD that act as an important indicator to evaluate and screen factors such as antioxidants that have an effect on UV stress resistance.
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* For research use only.