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Non-Melanoma Skin Cancer
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Irene De Francesco, Sean Whittaker, Stephen L. Morris
Xeroderma pigmentosum represents a group of autosomal recessive disorders, and the genetic basis of all xeroderma pigmentosum variants has recently been elucidated. The manifestations of xeroderma pigmentosum occur as a result of a defect in excision repair of UV-induced pyrimidine dimers.40,41 Nucleotide excision repair (NER) is one of the best-characterized DNA repair systems. The consequences of a defect in one of the NER proteins are manifested in three rare, recessive photosensitive syndromes: xeroderma pigmentosum, Cockayne’s syndrome, and a photosensitive form of brittle-hair disorder, trichothiodystrophy (TTD).
The Molecular Model and the Cytotoxic Action of UV Light
Published in K. H. Chadwick, Understanding Radiation Biology, 2019
UVB and UVC photons can induce deformational damage to a single strand of DNA, usually in the form of a pyrimidine dimer, where two thymidine nucleotide bases are adjacent to each other along one strand of the DNA. These pyrimidine dimers cause a deformation in the DNA strand and can be repaired using the undamaged DNA strand. This provides the complementary base sequence to guarantee the correct restoration of bases along the damaged strand at the deformation and gives perfect repair. This is similar to the perfect repair of DNA single strand breaks, induced by ionising radiation, but it takes longer.
Mutagenic Consequences Of Chemical Reaction with DNA
Published in Philip L. Grover, Chemical Carcinogens and DNA, 2019
It is not possible to consider chemical mutagenesis separately from DNA repair, because of the dual importance of repair in removing potentially mutagenic lesions from the DNA, and in converting such lesions into mutations. As a starting point, the author will try to describe our current knowledge of how DNA damage is accurately repaired by E. coli. Primarily, ultraviolet light (UV) induced damage will be discussed, and the responses of the bacterium to the whole spectrum of chemical carcinogens can then be considered as variations on a basic theme. UV is by far the most comprehensively investigated DNA damaging agent, and E. coli its most studied victim. As a reference agent, UV has several advantages, including easy administration, accurate dosimetry, and virtually instant treatment for kinetic studies. Moreover, the principal lesion is well characterized. Pyrimidine dimers are formed in which adjacent pyrimi-dines on the same DNA strand are joined by a cyclobutane type ring.38 Formation of the cyclobutane structure saturates the 5,6-double bond in the pyrimidine ring, causing it to become nonplanar.
Differential expression of flowering genes in Arabidopsis thaliana under chronic and acute ionizing radiation
Published in International Journal of Radiation Biology, 2019
Maryna V. Kryvokhyzha, Konstantin V. Krutovsky, Namik M. Rashydov
Early flowering of A. thaliana in response to drought stress, UV-C, and pathogens (for example, Fusarium oxysporum infection) was demonstrated recently (Takeno 2016). We observed that the low dose of 3 cGy irradiation exposure also promotes early flowering in A. thaliana plants. Published studies have also shown that the FT gene could be involved in stress-induced flowering (Takeno 2012). However, we did not observe its increased expression in earlier flowering (King et al. 2008). The photoperiodic CO gene was upregulated and followed by flowering acceleration. Our study has shown that the effects of the 17 cGy chronic and 15 Gy acute irradiations were similar to the UV-B effect (Ali et al. 2015). The short-wavelength UV light can cause photolesions and cyclobutane–pyrimidine dimers in DNA and its structural disintegration (Brem et al. 2017; Chen et al. 2017).
Assessing the impact of low level laser therapy (LLLT) on biological systems: a review
Published in International Journal of Radiation Biology, 2019
Ruwaidah A. Mussttaf, David F. L. Jenkins, Awadhesh N. Jha
It has been reported that the photo-reactivating enzyme (DNA photolyase) distinguishes one type of DNA damage as its substrate (i.e. the cyclobutane-type pyrimidine dimer), and combines with these dimers in the dark (Smith 1991). However, when exposing the enzyme-substrate complex to visible light, the enzyme uses the absorbed energy of light to split the dimer to produce repaired (original) DNA. Mbene (2008) treated wounded human skin fibroblast cells by He-Ne laser with 5 J/cm2 and 16 J/cm2 doses. Irradiation with 5 J/cm2 and 16 J/cm2 showed insignificant change in DNA damage, as determined by alkaline comet assay, at 1 h when compared to their respective controls. However, a significant decrease in DNA damage at 24 h incubation due to the mechanism of DNA repair was shown (Mbene 2008).
Prospects of topical protection from ultraviolet radiation exposure: a critical review on the juxtaposition of the benefits and risks involved with the use of chemoprotective agents
Published in Journal of Dermatological Treatment, 2018
Nilutpal Sharma Bora, Bhaskar Mazumder, Pronobesh Chattopadhyay
Pyrimidine dimers are the most representative DNA lesion, which represents the genotoxic effects of the UVB radiation and are mainly mediated by the direct absorption of photons by DNA (38). Exogenous molecules (eg, photosensitizing drugs) also get activated by sunlight, which can increase the risk of photocarcinogenesis. Some of these molecules react directly with DNA (eg, psoralens), whereas others cause damage by generating a local oxidative stress (eg, antibiotics and nonsteroidal anti-inflammatory drug) (39). Photosensitization of DNA by chemicals can also increase the risk of photocarcinogenesis; for example, psoralen plus UVA therapy or antibiotic treatment such as fluoroquinolones (38).