Some aspects of the effect of ultraviolet radiation on animal cells

Djelovanje ultravioletnog zračenja na animalne stanice prikazano je i prodiskutirano s nekoliko različitih aspekata koji zajedno omogućuju potpunije razumijevanje ove problematike; od fotokemijskih promjena na molekularnoj razini, promjena u biokemijskim procesima metabolizma, do razine biološkog funkcioniranja stanice i preživljenja nakon zračenja. Nastajanje letalnih posljedica i fenomen reparacije oštećenja stvorenih u animalnim stanicama nakon ultravioletnog zračenja prikazano je uz isticanje makromolekularne osnove za promjene u ozračenoj stanici, povezanosti s indukcijom karcinogeneze i sličnosti s reparatornim procesima do kojih dolazi nakon oštećenja DNA uslijed drugih uzroka. Razmatrane su aktuelne koncepcije i ideje koje bi mogle dovesti do novih eksperimentalnih rezultata i boljeg razumijevanja djelovanja ultravioletne svjetlosti na animalne (uključujući i humane) stanice.Various aspects of the effect of ultraviolet light on mammalian cells grown in vitro are shown and discussed: from photochemical and photobiological aspects of cellular radiobiology to its pertinence to carcinogenesis. The macromolecular basis of the changes in irradiated cells is underlined. An attempt was made to survey some current concepts and ideas that may lead to better understanding of the effects of ultraviolet light on the living mammalian (including human) cells. Although UV-irradiation induces various kinds of molecular damage in mammalian cells two main types of photochemical lesions seem to be critical for the cell survival: pyrimidine dimers and DNA-protein crosslinking. The kinetics of dimer induction, simple in its proportionality with UV exposure, is followed by complex interactions of metabolic processes and repair pathways. The existence of two different modes in removal of pyrimidine dimers from the DNA divides mammalian cells in two main groups. The first group (in which human cells are included) has developed enzymatic mechanism for excising damaged parts from corresponding DNA; the second group (rodent cell lines) has formed the mechanism for postreplication repair of photochemical lesion. UV exposure is followed by intensive reparation activity thus attempting to remove the photochemical damage hindering normal metabolic activities. There are many variations and alternative pathways in these processes which are embracing DNA, various enzymes and other proteins and factors. The repair of each of UV-induced dimers undoubtedly does not function according to the same mechanical cliche, In the first phase of intensive reparation activity the mammalian cell certainly can not remove the complete photochemical damage induced by UV irradiation; perhaps cca 50-70°/o of dimers are repaired in the first few hours after irradiation. To the contrary, it was demonstrated that these cells posses enzymatic mechanisms capable of repairing even greater number of dimers than that induced by exposures on the limit lethality (66). However, in the chromatin of cells there is a portion of photochemical damage that can not be approached by repair mechanism. Nevertheless, mammalian cells can survive in spite of the existence of the fraction of unrepaired dimers in their DNA which was untouched during the first hours after the irradiation. This is managed by bypass mechanism which temporarily enables the cells to »ignore« the existence of fraction of photochemical damage in their DNA. Those remaining dimers are gradually removed in a period of few days. In spite of all its complexity, the phenomena of UV induction of pyrimidine dimers and their repair can not exclusively comprehend mammalian cell tilling by UV light, specially survival variations in distinct phases of the cell cycle. The induction of another photochemical lesion, DNA-to-protein crosslinking, varies through the cell cycle in the similar manner as the cell survival, what indicates the biological importance of this type of damage. Many particularities connected with this type of lesion are still unclear, but there seem to be no repair of DNA-protein crosslinks. In addition with the critical number of unrepaired pyrimidine dimers, DNA-to-protein crosslinking therefore could have the principal role in UV-induced cell killing