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The DNA of a cell is vulnerable to the damaging effect of oxidative free radicals produced as byproducts of cellular metabolism. DNA damage occurring in oocytes, if not repaired, can be lethal and result in reduced fecundity and loss of potential progeny.
In mammalian females the period of arrest may last for years. During this period of arrest, oocytes are subject to spontaneous DNA damage including double-strand breaks. However, the oocytes can efficiently repair DNA double-strand breaks, allowing the restoration of genetic integrity and the protection of offspring health. [8]
The central role of DNA damage and epigenetic defects in DNA repair genes in carcinogenesis. DNA damage is considered to be the primary cause of cancer. [17] More than 60,000 new naturally-occurring instances of DNA damage arise, on average, per human cell, per day, due to endogenous cellular processes (see article DNA damage (naturally occurring)).
Similar to S Phase, G2 experiences a DNA damage checkpoint. The cell is once more examined for sites of DNA damage or incomplete replication, and the kinases ATR and ATM are recruited to damage sites. Activation of Chk1 and Chk2 also transpire, as well as p53 activation, to induce cell cycle arrest and halt progression into mitosis.
Bile acids cause DNA damage, including oxidative DNA damage, double-strand DNA breaks, aneuploidy and chromosome breakage. [55] High-normal levels of the bile acid deoxycholic acid cause apoptosis in human colon cells, [ 56 ] but may also lead to colon cancer if repair and apoptotic defenses are insufficient.
Cancer is caused by genetic changes leading to uncontrolled cell growth and tumor formation. The basic cause of sporadic (non-familial) cancers is DNA damage and genomic instability. [1] [2] A minority of cancers are due to inherited genetic mutations. [3] Most cancers are related to environmental, lifestyle, or behavioral exposures. [4]
Radiolysis of intracellular water by ionizing radiation creates peroxides, which are relatively stable precursors to hydroxyl radicals. 60%–70% of cellular DNA damage is caused by hydroxyl radicals, [3] yet hydroxyl radicals are so reactive that they can only diffuse one or two molecular diameters before reacting with cellular components.
Mediator of DNA damage checkpoint protein 1 is a 2080 amino acid long protein that in humans is encoded by the MDC1 gene [5] [6] [7] located on the short arm (p) of chromosome 6. MDC1 protein is a regulator of the Intra-S phase and the G2/M cell cycle checkpoints and recruits repair proteins to the site of DNA damage.