UV-Induced DNA Damage and Repair: A Powerful Light Trapping System in DNA in Order to Convert Light Energy into Biochemical Signals

Summary

Photons participate in many atomic and molecular interactions and changes. Recent biophysical research has shown the existence of photons in biological tissue and plants, animal and human cells emit a very weak radiation which can be readily detected with an appropriate photomultiplier system. Although the emission of this radiation is extremely low in mammalian cells, it can be efficiently induced by ultraviolet light. Ultraweak radiation in human fibroblasts can also be enhanced by a brief illumination with an ordinary fluorescent light source. The nature of the emitted light can then be examined as rescattered emission, an experimental approach which allows the investigation of ultraweak re-emission patterns in the differentiation system of normal- and DNA repair-deficient Xeroderma Pigmentosum (XP) fibroblasts. We have reported that postmitotic XP-fibroblasts lose the storing capacity of ultraweak photons which are efficiently trapped in normal cells. Thus, it is evident that there exists an important difference between normal and XP cells and this suggests that there is an effective intracellular mechanism of photon trapping in normal human cells. It is proposed that nucleic acids may play via pyrimidine dimer formation, a similiar role of light trapping as is known for vitamin A in the retinal isomerization reaction found in the light driven photon conversion process of the eye. This light-trapping system can influence metabolic and cellular events by triggering amplification mechanisms and promoting photochemical processes long after exposure to light via excision repair as shown recently by Gilchrest and co-workers (1994) for induced melanogenesis via excised UV-induced pyrimidine dimer molecules.