Cyclobutane-type pyrimidine dimers participate as important factors in ultraviolet-induced lethality, mutagenicity and tumorgenicty. Substantial efforts have been made in recent years to understand the induction of pyrimidine photodimers and their repair in human skin cells exposed to low fluences of UV-light. Dimers are efficently induced after UVC and UVB- irradiation, but these photoproducts are even produced in DNA of human skin in vivo after UVA irradiation. By developping a highly sensitive immunohistochemistry dimer detection assay, we confirm that UVA radiation induces substantial amounts of these DNA-changes in the epidermis and this enhanced immunohistochemistry technique detects them even down to the reticular dermis. A considerable number of these photodimers were also seen in non-irradiated control skin up to 2 cm away from the irradiation site which persist for at least two days postirradiation time. Recent biophysical research has shown the existence of ultraweak photons in biological tissue. UVA is inducing in DNA-excision repair deficient XP cells such very weak cell radiation. It is now established that plants, animal and human cells emit a very weak radiation which can be readily detected with an appropriate photomultiplier system. Although the emission is extremely low in mammalian cells, it can be efficiently induced by ultraviolet light. Photons in the visible range are coupled with radical reactions while photons in the UV are linked with the DNA as the source. These results sustain the hypothesis that pyrimidine dimer formation and excision repair as well as ultraweak photon emission seem be involved in a type of intra- and extracellular photobiostimulation and may be important triggers of UV-induced signal pathways expressing epidermal communication.
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