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Oxidative DNA damage
According to Henle and Linn (1997), reactive oxygen species, also known as ROS, are typical byproducts of the electron transport chain (ETC) during cellular respiration in aerobic organisms. ROS are also derived from catabolic oxidases, anabolic processes and peroxisomal metabolism.
Abstract
Living things are constantly subjected to a wide variety of DNA-damaging agents, any one of which has the potential to have an effect on health and to modulate disease states. However, robust DNA repair and damage-bypass mechanisms faithfully protect the DNA by either removing the damage or tolerating it in order to ensure an overall survival. This is done in order to ensure an overall survival. Variations in this fine-tuning are known to destabilise cellular metabolic homeostasis, which can be seen as an example in a variety of cancers, in which the disruption or deregulation of DNA repair pathways results in genome instability. Because biological, physical, and chemical agents that are used on a regular basis can have an effect on human health, testing for their genotoxicity and regulating their application have become increasingly important. In this introductory review, we will provide insights into the molecular basis of genotoxicity in cells to lay the foundation for subsequent articles that will be published in this issue. Specifically, we will delineate mechanisms of DNA damage and the counteracting repair/tolerance pathways.
Base excision repair, mismatch repair, nucleotide excision repair, single and double strand break repair, translesion synthesis, and telomeres are some of the keywords that can be associated with this type of repair.
Different Kinds of DNA Damage
On the basis of where the DNA damage originated, it is possible to divide it into two primary categories: endogenous and exogenous. The majority of the endogenous DNA damage is caused by the chemically active DNA undergoing oxidative and hydrolytic reactions, respectively, with water and reactive oxygen species (ROS) that are naturally present within cells. These reactions are responsible for the majority of the endogenous DNA damage. Such inherently predisposed reactions of DNA with molecules from its immediate surroundings fuel the development of hereditary diseases and sporadic cancers [Visconti and Grieco, 2009; Reuter et al., 2010; Perrone et al., 2016]. [Visconti and Grieco, 2009; Reuter et al., 2010; Perrone et al., 2016] [Visconti and Grieco, 2009; Damage to the DNA that is caused by exogenous sources, on the other hand, can be caused by environmental, physical, or chemical agents. Some examples of this include alkylating agents, crosslinking agents, ultraviolet and ionising radiation, and so on. In this section, we will provide a brief summary of the primary endogenous and environmental agents that produce the various classes of DNA damage that then become substrates for the specific DNA repair pathways that will be discussed in the subsequent section. These agents can be found in both the body and the environment.
Conclusion
The aesthetic appeal of the DNA double helix initially hindered notions of DNA mutation and repair, which would necessarily interfere with its pristine state. This is because DNA mutation and repair would require the double helix to be altered. Since then, however, it has been established that DNA is continuously vulnerable to damage, and each cell possesses a toolbox of mechanisms to act in response to any such injury.
