China
Africa
Explore chapters and articles related to this topic
Introduction to Cancer
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
The UV band, which is invisible to the human eye, constitutes one component of the spectrum of sunlight and represents approximately 3% of all the solar radiation reaching the Earth’s surface. Three types of UV light have been identified. One of these, UV-C (200 to 290 nm), is generally thought to be the most carcinogenic. UV-B (290 to 320 nm) causes the most sunburn, and UV-A (320 to 400 nm), which can be up to 1,000 times stronger than UV-B, is able to penetrate underlying tissues of the skin leading to “photo-aging” damage. For many years it was thought that UV-A could not cause any lasting damage. However, more recent studies strongly suggest that it may also enhance the development of skin cancers. Fortunately, the ozone layer absorbs most of the more carcinogenic UV-C radiation, although there is presently concern that depletion of the ozone layer through the release of chlorofluorocarbons used in the air conditioner and refrigeration industries and in the production of Styrofoam insulation may increase the intensity of UV-C at the Earth’s surface in the future. UV radiation occurs at a similar wavelength to the region of maximum absorbance by DNA (i.e., 260 nm), and the major damage is intrastrand covalent linkage of adjacent pyrimidines (usually thymines) to form so-called thymine dimers. These thymine dimers create distortions in the DNA helix and can block replication and transcription, thus leading to tumorigenesis.
Topical and Systemic Photoprotection of Human Skin Against Solar Radiation
Published in Henry W. Lim, Nicholas A. Soter, Clinical Photomedicine, 2018
The UVB band extends from 290 to 320 nm. It is often referred to as sunburn-producing radiation, mid-ultraviolet radiation, or erythemal band. Exposure to UVB radiation is the principal cause of the sunburn reaction. It is also the most effective band in stimulating pigmentation (melanogenesis or tanning) in the skin. In individuals with skin types I–IV, the MED of UVB is approximately 20–60 mJ/cm2 (Table 4). The intensity of UVB radiation decreases with increasing latitude from 0 to 90 degrees north and south. Fair-skinned individuals living on the equatorial belt (0–10 degrees N) may obtain one MED dose in about 10 min (11 am to 1 pm); those living in subtropical regions (10–25 degrees N,S) may obtain one MED dose in 10–15 min, and those living between 25 and 35 degrees N,S may obtain one MED dose in about 15–20 min during the summer months. Exposure of human skin to multiple MEDs (8–15 times MED) for a prolonged period can cause a marked sunburn reaction that can be painful and lead to severe edema and blistering response. The UVB-induced erythema reaction is maximal in intensity between 20 and 24 hr after exposure and appears to be caused by the generation of eicosanoids. Exposure to UVB radiation results in immediate damage to DNA, RNA, and proteins of epidermis and dermis. The damage to DNA in the form of thymine dimers and strand breaks can contribute to mutation and skin carcinogenesis.
DNA Repair During Aging
Published in Alvaro Macieira-Coelho, Molecular Basis of Aging, 2017
Genomes containing dsDNA have built-in informational redundancy because of complementarity. Damage within a single strand can be repaired by excising the damage and replacing the lost information by copying. One of the best-investigated processes that can serve as an example for all excision repair mechanisms is the repair of a thymine dimer in phage T4.41,42
Skin impacts from exposure to ultraviolet, visible, infrared, and artificial lights – a review
Published in Journal of Cosmetic and Laser Therapy, 2021
Juliana Yuka Furukawa, Renata Miliani Martinez, Ana Lucía Morocho-Jácome, Thalía Selene Castillo-Gómez, Vecxi Judith Pereda-Contreras, Catarina Rosado, Maria Valéria Robles Velasco, André Rolim Baby
An investigation published by Liebel et al. (3) demonstrated an increase in intracellular hydrogen peroxide related to the production of ROS, which can induce the formation of MMPs and epidermal pro-inflammatory cytokines, such as IL-1 alpha, IL-6 and IL-8, after stimulation by visible light in human epidermis equivalents. The same test was carried out under the stimulation of UV radiation, which produced tumor necrosis factor alpha (TNF-alpha), which did not occur in induction with visible light. Furthermore, visible light also did not induce the formation of thymine dimers, related to skin cell DNA damage. Visible light can also be used in treatment therapies for atopic dermatitis, eczema, and antimicrobial photodynamic therapy, due to its absorption by the skin’s chromophores (3,26).
Mitochondrial DNA damage in the hair bulb: can it be used as a noninvasive biomarker of local exposure to low LET ionizing radiation?
Published in International Journal of Radiation Biology, 2020
Rita Hargitai, Päivi Roivainen, Dávid Kis, Jukka Luukkonen, Géza Sáfrány, Jan Seppälä, Tünde Szatmári, Tuomas Virén, Kristiina Vuolukka, Sisko Salomaa, Katalin Lumniczky
A novel possibility for a biodosimetry tool could be the analysis of damage in mtDNA with real-time polymerase chain reaction (PCR). Advantages of the real-time PCR technique include its sensitivity, speed, and the requirement of only 1–2 nanogram of DNA. One way to detect mtDNA damage is using the long-range real-time PCR method, which is based on the principle that several kinds of DNA damages (strand breaks, abasic sites, thymine-dimers) can slow down or block the progression of DNA polymerase (Santos et al. 2006; Edwards 2009; Rothfuss et al. 2010; Lehle et al. 2014). Recently developed high-performance DNA polymerase mixtures (highly processive polymerase with thermostable proofreading enzyme) and next-generation intercalating dyes (e.g. EvaGreen) permit rapid and efficient amplification of even very long DNA fragments (Edwards 2009).
Sunlight radiation as a villain and hero: 60 years of illuminating research
Published in International Journal of Radiation Biology, 2019
Julia Montelin Powers, James Edward John Murphy
Although it was known at this time that ultraviolet light caused skin malignancies (Howell 1960), the mechanisms at work had not yet been fully elucidated (Mackie and McGovern 1958); the effects of UV on DNA were only being investigated in the 1960s, with the discovery that UVB produced mutagenic DNA thymine dimers (Setlow and Setlow 1962). Key work in understanding the penetration of light into human skin made it clear that the shorter wavelengths of UVB did not penetrate to the skins germ-cell (sic) layer while the longer UVA radiation could reach subcutaneous tissue where cells were proliferating (Bachem and Reed 1931). The differences between deeper basal cell and squamous cell carcinomas were also being studied (Pinkus 1959), with a focus on the erythemal UVB rays (Macdonald 1959); a connection between adverse effects to skin and ‘harmless’ UVA had not yet been made (Knox et al. 1960).