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The system involves the RecA protein (Rad51 in eukaryotes). The RecA protein, stimulated by single-stranded DNA, is involved in the inactivation of the repressor of SOS response genes thereby inducing the response. It is an error-prone repair system that contributes significantly to DNA changes observed in a wide range of species.
Epigenetic alterations can accompany DNA repair of oxidative damage or double-strand breaks. In human cells, oxidative DNA damage occurs about 10,000 times a day and DNA double-strand breaks occur about 10 to 50 times a cell cycle in somatic replicating cells (see DNA damage (naturally occurring)). The selective advantage of DNA repair is to ...
XthA (exonuclease III, a DNA repair enzyme) and KatE (catalase) are known to play important roles in the defense against oxidative stress but KatF regulon genes are not induced by oxidative stress. [2] There is an overlap between oxidative stress response and other regulatory networks like heat shock response, SOS response.
More than 100 types of oxidative DNA damage have been characterized, and 8-oxodG constitutes about 5% of the steady state oxidative damages in DNA. [18] Helbock et al. [ 14 ] estimated that there were 24,000 steady state oxidative DNA adducts per cell in young rats and 66,000 adducts per cell in old rats.
DNA oxidation is the process of oxidative damage of deoxyribonucleic acid.As described in detail by Burrows et al., [1] 8-oxo-2'-deoxyguanosine (8-oxo-dG) is the most common oxidative lesion observed in duplex DNA because guanine has a lower one-electron reduction potential than the other nucleosides in DNA.
Other DNA damaging, cancer-causing agents include asbestos, which can cause damage through physical interaction with DNA or by indirectly setting off a reactive oxygen species, [10] excessive nickel exposure, which can repress the DNA damage-repair pathways, [11] aflatoxins, which are found in food, [9] and many more.
It is involved in oxidative DNA damage repair and is part of the base excision repair pathway. The enzyme excises adenine bases from the DNA backbone at sites where adenine is inappropriately paired with guanine, cytosine, or 8-oxo-7,8-dihydroguanine, a common form of oxidative DNA damage. The protein is localized to the nucleus and mitochondria.
The adaptive response is a DNA damage response pathway prevalent across bacteria that protects DNA from damage by external agents or by errors during replication. [1] [2] It is initiated specifically against alkylation, particularly methylation, of guanine or thymine nucleotides or phosphate groups on the sugar-phosphate backbone of DNA.