Notes on Genetic and Radiation Control of Senescence
Nate F. Cardarelli in The Thymus in Health and Senescence, 2019
Ultraviolet (UV) radiation has long been recognized as an inducer of cell mutation, leading to a number of effects, including carcinogenesis.290–292 Middle and far UV radiation destroys various bonds in DNA, causing a plethora of mutations.293 Solar radiation below 2900 Å, however, does not penetrate the atmospheric barrier, nor are there any but the most miniscule sources of the Schumann UV at the earth’s surface. Thus it likely plays no role in cueing endogenous rhythms. Ultraviolet radiation at low dosages administered in late G1 or early S phase delays mitosis in vitro.294 In Chinese hamster cells G2 and M phases are highly UV resistant, while S phase is sensitive.295 UV damage to DNA seems to be concentrated at pyrimidine sites.293,296 Repair is effected by various endonucleases.296 Oddly enough, UV-caused genetic damage, normally fatal to the cell, is repairable by enzymes activated by visible light. This photoreactivation effect has been observed in various species.298 DNA effects are greatest in the UVB region (2900 to 3200 Å).299,300
Photoimmunology: Effects of Ultraviolet B Radiation on Cutaneous Photocarcinogenesis and Allergic Contact Sensitivity
Henry W. Lim, Nicholas A. Soter in Clinical Photomedicine, 2018
Studies with the South American opossum (whose cells contain photoreactivating enzyme, which can repair spontaneously UV-induced DNA damage) have demonstrated that both UVB-induced morphologic alterations in Langerhans cells and UVB-induced suppression of allergic contact sensitivity can be reversed by exposure to photoreactivating light (33). These findings suggest that damage to DNA is involved in these UVB effects, and that such DNA damage can be repaired by photoreactivation in the opossum. On the other hand, photoreactivation studies in humans have failed to show reversal of both of these UVB effects (34); it should also be noted that the existence of photoreactivating enzyme in humans remains controversial.
Mutagenic Consequences Of Chemical Reaction with DNA
Philip L. Grover in Chemical Carcinogens and DNA, 2019
Photoreactivation and excision repair remove the damage from the DNA. The other two processes in E. coli, recombination repair and error-prone repair, do not do this; instead they enable functional new DNA to be formed, despite the presence of damage in the template.
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
A study by da Silva Sergio et al. (2012) used an AlGaInP laser with a power output of 10 mW and with continuous or pulsed mode of irradiation. They found that low-intensity red laser radiation could induce DNA lesions via oxidative mechanisms. Moreover, it was found that the survival mechanism against harmful radiation could be activated or induced after irradiation with monochromatic red light (da Silva Sergio et al. 2012). Kohli et al. (2001) examined E. coli cells with a He-Ne laser at 632.8 nm. They observed that irradiation with low-level He-Ne lasers induces photolyase gene (phr) and DNA repair genes investigated by phr gene expression assay. The magnitude of induction relies on fluence rate of the He-Ne laser and the time of incubation post irradiation. The study concluded that the stimulation of DNA repair may explain the higher survival cell against UV radiation (Kohli et al. 2001).
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
Another avenue which is being explored by researchers is the inclusion of topical antioxidants and DNA repair stimulants which prove to be beneficial for improving the photoprotective properties of sunscreen formulations. Antioxidants that can be administered via the dermal route, like reservatrol, flavonoids, and green tea extracts may prove to be advantageous in reducing skin damage caused by UV rays, despite the fact that these are chemically unstable and poorly diffuse into the epidermal layer (100–103). T4 endonuclease and photolyase which are two important DNA repair enzymes have proven to decrease the UV-related DNA damage (104–106). Thymidine dinucleotides stimulate the DNA repair response mechanism if administered prior to UV exposure and helps in curbing the DNA damage caused by UV radiation (107).
Efficacy of new class I medical device for actinic keratoses: a randomized controlled prospective study
Published in Journal of Dermatological Treatment, 2021
Federica Veronese, Elisa Zavattaro, Gionathan Orioni, Gianluca Landucci, Vanessa Tarantino, Chiara Airoldi, Paola Savoia
In the last few years, some studies have shown that the addition of xenogenic DNA repair enzymes (i.e. photolyase) to traditional sunscreens may reduce UVR-induced cyclobutane pyrimidine dimers (CPDs) formation more than the sunscreens alone (18–20). CPDs represents the first cause of alterations in the structure of DNA and then of mutations in skin tumorigenesis (21,22).