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The arrest of ooctyes at the four genome copy stage appears to provide the informational redundancy needed to repair damage in the DNA of the germline. [26] The repair process used likely involves homologous recombinational repair. [26] [27] [28] Prophase arrested oocytes have a high capability for efficient repair of DNA damages. [27]
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)).
Degenerated oocytes are classified as damaged oocytes or oocytes without a zona pellucida. [6] Dysmorphic oocytes are oocytes with abnormal physical characteristics, for example multiple nuclei. [7] EFS is a condition occurring when no oocytes are produced from the mature follicle after ovulation is induced in cycles of in vitro fertilisation ...
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]
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.
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