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Stochastic Model to Explain the Biology and Epidemiology of the Ultraviolet Induction of Skin Cancer
Published in Ovide Arino, David E. Axelrod, Marek Kimmel, Mathematical population dynamics, 2020
When damage to the DNA occurs, the cell cycle is usually interrupted while the cell responds with its repair mechanisms. One such mechanism, called photoreactivation, needs UV-Α radiation to simulate photoenzymes found in the cell (Kelner, 1949). These enzymes are capable of repairing just one type of DNA damage, base dimers. Photoreactivation works speedily and is highly efficient with an error rate on the order of 10−10 (Harm, 1980). Photoenzymes have not yet been found in mammalian epidermal cells, although they have been discovered in some cells in the dermis. Another efficient DNA repair mechanism which works more slowly but may repair general types of damage (not just dimers) is called excision repair (Setlow, 1968). Excision repair is actually a class of mechanisms that has been discovered in every species for which an attempt has been made to find it. After replication has occurred on either side of a lesion in a DNA strand, the cell may respond with its postreplication gap repair system (Howard-Flanders, 1968). Postreplication repair, again the name for a class of repair systems, acts as a cell’s last ditch effort to fix the DNA damage and is fairly error prone.
A male germ cell assay and supporting somatic cells: its application for the detection of phase specificity of genotoxins in vitro
Published in Journal of Toxicology and Environmental Health, Part B, 2020
Khaled Habas, Martin H. Brinkworth, Diana Anderson
Endogenous and exogenous chemicals, other physical and biological agents affect the genome of spermatozoa. DNA integrity of germ cells is essential for making normal motile spermatozoa (de Rooij and Russell 2000; Simhadri et al. 2014). The genomic integrity of the spermatozoa is maintained and protected by DNA repair mechanisms. These include nucleotide excision repair, base DNA mismatch repair, excision repair, double strand break repair, and post-replication repair. Failure in these mechanisms might lead to arrest of spermatogenesis or abnormal recombination, resulting in male infertility (Gunes, Al-Sadaan, and Agarwal 2015). Infertility is a condition of the reproductive system where genetic factors and environmental causes may also be involved. Although some specific mutations were identified, other factors related to sperm defects remain unidentified (Venkatesh, Suresh, and Tsutsumi 2014). Spermatogonial stem cells (SSCs) are responsible for the protection of spermatogenesis throughout male adult reproductive life. Moreover, SSCs require accurate expression of genes for the monitoring and regulation of germinal mitosis, meiosis, and apoptosis and maintenance of genomic integrity in spermatogenesis. Male germ cells need to be protected against DNA damage and mutations to maintain reproduction and species survival. Maintenance of genetic stability requires both extremely precise DNA replication processes and mechanisms for the removal of a variety of DNA damage. Damage in male germ cell as key morphological events is an indicator after administration of genotoxic chemicals (Vidal and Whitney 2014). As a consequence of exposure to genotoxic chemotherapy drugs, histopathological changes occur in the testis (Meistrich 1986). These alterations are reliant upon chemotheraptic drugs used and cell types being exposed. In the mammalian testis, different target cells identified for chemotherapy agents are germ cells (spermatogonia, spermatocytes, and spermatids) and somatic cells (Leydig and Sertoli cells) (Habas, Anderson, and Brinkworth 2016). Numerous studies in animals demonstrated that phase specificities in male germ cells selectively may be targeted by specific reproductive cytotoxic agents both in vivo and in vitro (Anderson et al. 1981; Habas, Brinkworth, and Anderson 2017c) Table 1.