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Malignant diseases of the skin
Published in Rashmi Sarkar, Anupam Das, Sumit Sethi, Concise Dermatology, 2021
Anupam Das, Yasmeen Jabeen Bhat
Management is directed to genetic counselling, removal of neoplastic lesions as they occur, and prevention of further photodamage by advice and sunscreens. Addition of DNA repair enzymes (photolyase and endonuclease) to traditional sunscreens may lessen UVR-induced molecular damage. The use of systemic retinoids may reduce the rate of development of new cancers.
Mitochondrial Genome Damage, Dysfunction and Repair
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Kalyan Mahapatra, Sayanti De, Sujit Roy
Direct reversal repair represents the simplest pathway and also an alternative to photoreactivation of cyclobutane pyrimidine dimers or CPD by photolyase in E. coli without cleaving the phosphodiester chain (Sancar, 2008). Although mammalian mitochondria contain homologue of photolyase, transcriptional repressors, cryptochrome1 and 2 (CRY1 and CRY2) (Kobayashi et al., 1998), they are mainly involved in regulating the circadian rhythm. In contrast to yeast photolyase activity, which revert the UV induced damage to DNA (Pasupathy et al., 1992; Yasui et al., 1992), no direct evidence for reversal of UV induced damage could be detected in mitochondria. Along with the yeast, photolyase activity is evidenced in plant mitochondria (Takahashi et al., 2011) and Xenopus mitochondria (Ryoji et al., 1996). It is generally seen that higher eukaryote mitochondria do not possess the photolyase activity.
DNA Repair During Aging
Published in Alvaro Macieira-Coelho, Molecular Basis of Aging, 2017
One type of dimer results from covalent linkage between two neighboring pyrimidine bases and forms a cyclobutane ring. The DNA photolyase directly opens the ring in a light-dependent process.48 This photolyase was found in bacteria, plants and animals — with the highest significance probably in plants. Interestingly, this enzyme was found in internal organs which never get in contact with exogenous UV. Possibly it is used to remove damages caused by endogenous UV that is produced together with visible light inside the cells.49
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 different photoprotection strategies in preventing actinic keratosis new lesions after photodynamic therapy. The ATHENA study: a two-center, randomized, prospective, assessor-blinded pragmatic trial
Published in Current Medical Research and Opinion, 2019
Paolo Sergio Pavone, Silvia Lovati, Giuseppe Scarcella, Massimo Milani
In the present study (ATHENA study; trial number: ISRCTN16168548) we evaluated the efficacy and tolerability of a topical product based on 0.8% piroxicam and 50+ solar filters (ACTX), applied twice a day as sequential therapy after conventional or daylight PDT (C-PDT; DL-PDT) on the evolution of AK lesions number compared to the use of very high photoprotection products commonly used in this clinical setting (SPF50+ or SPF100+ associated with photolyase, a DNA-repairing enzyme; Defence Sun 50+, Bionike Italy; Eryfotona AK, Isdin Spain) (Standard Sunscreens: SS group).