UV damage

Alkyiresorcinols Protect the DNA from UV-Damage In Vitro and In Vivo Models... 

Thus, the AR directly protect DNA from the UV-damage. This is manifested in the saving of the total amount of this biopolymer, preventing its deep degradation due to formation of double-stranded breaks, as well as preventing the single -stranded breaks without transition of supercoiled into the relaxed circular form of DNA. Evidence of effects increased with length of the alkyl radical of the AR molecule and with AR concentration increase. 

Electron donation to nucleobases is a fundamental process exploited by nature to achieve the efficient repair of UV induced lesions in DNA [27, 28]. Nature developed to this end two enzymes, CPD photolyases and (6-4) photolyases, which both inject electrons into the UV damaged DNA bases [29, 30]. Both enzymes are, in many species, including plants, essential for the repair of the UV-light induced DNA lesions depicted in Scheme 1 [31]. 

On the other hand, the observation that 95% of the UV induced base substitution mutations arose at the very sites (pyrimidine-pyrimidine sequences) where the major fraction of UV damage is deposited suggested that at least the UV induced mutations were targeted (24). 

Pasheva, E.A., Pashev, I.G., and Favre, A. (1998) Preferential binding of high mobility group 1 protein to UV-damaged DNA. Role of the COOH-terminal domain. J. Biol. Chem. 273, 24730-24736. 

Gaillard, H., Fitzgerald, D.J., Smith, C.L., Peterson, C.L., Richmond, T.J., and Thoma, F. (2003) Chromatin remodeling activities act on UV-damaged nucleosomes and modulate DNA damage accessibility to photolyase. J. Biol. Chem. 278, 17655-17663. 

Dixon, P., Weinig, C., and Schmitt, J., Susceptibility to UV damage in Impatiens capensis (Balsaminaceae) testing for opportunity costs to shade-avoidance and population differentiation. Am. J. Bot, 88, 1401, 2001. 

Most microorganisms have redundant pathways for the repair of cyclobutane pyrimidine dimers— making use of DNA photolyase and sometimes base-excision repair as alternatives to nucleotide-excision repair—but humans and other placental mammals do not. This lack of a back-up to nucleotide-excision repair for the removal of pyrimidine dimers has led to speculation that early mammalian evolution involved small, furry, nocturnal animals with little need to repair UV damage. However, mammals do have a path-... 

This example inspired searches for radiation sensitive mutants in yeast. The way was led by Nakai and Matsumoto (1967) who isolated one mutant, UV which was very sensitive to ultraviolet and a second, Xj sensitive to X-rays. They went one step further than isolation and survival curves by making the double-mutant and showing that like double mutants of recA and uvr A in E. coli it was much more sensitive to UV than either single mutant alone. This was the first demonstration of the existence of more than one type or pathway of DNA repair of UV damage in yeast, and inspired the later work of Game and Cox (1972 1973 1974), Brendel and Haynes (1973) and Louise Prakash (1993) in the genetic analysis of pathways of repair in yeast. This led to the classification of the many mutant loci into epistasis groups, which are defined as those mutants which, when combined in the same strain, are no more UV-sensitive than the most sensitive of the two when alone. 

A number of studies are concerned with the free-radical reactions of typical nucleobase lesions. For example, the cyclobutane-type Thy dimer can be split by one-electron reduction [Heelis et al. 1992 reactions (307) and (308)], a process that is relevant to the repair of this typical UV-damage by the photoreactivating enzyme (photolyase, for a review see Carrell et al. 2001, for the energetics of the complex reaction sequence, see Popovic et al. 2002). At 77 K, the dimer radical anion is sufficiently long-lived to be detectable by EPR (Pezeshk et al. 1996). 

Resistance to one form of radiation does not necessarily convey protection from other forms. Almost all organisms are prone to UV damage because the macromolecules that propagate genetic information (DNA) absorb UV radiation. For example, the experiments in the Atacama Desert cited in the previous section were done in the dark (shade). Direct exposure to UV radiation in these experiments killed all organisms within hours (Dose et al. 2001). 

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