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Thus it appears that a process evolved to avoid this vulnerability of germline DNA. It was proposed that, in order to avoid damage to the DNA genome of the oocytes, the metabolism contributing to the synthesis of much of the oocyte's constituents was shifted to other maternal cells that then transferred these constituents to oocytes.
Oocytes are immature egg cells that develop to maturity within a follicle in the ovary. Oocyte abnormalities can occur due to several factors, including premature ovarian insufficiency (POI) , other maturation abnormalities, maternal ageing, and mitochondrial abnormalities.
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]
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 allow the cell to survive in the face of DNA damage.
When there is too much damage, apoptosis is triggered in order to protect the organism from potentially harmful cells.7 p53, also known as a tumor suppressor gene, is a major regulatory protein in the DNA damage response system which binds directly to the promoters of its target genes. p53 acts primarily at the G1 checkpoint (controlling the G1 ...
In aged and chemotherapy treated females, oocytes and follicles are depleted by apoptosis (programmed cell death) leading to ovarian failure. DNA damage-induced oocyte apoptosis depends on the efficiency of the DNA repair machinery that in turn declines with age. Survival of oocytes following chemotherapy or aging can be enhanced by increased ...
However, it has been proposed that the arrest of oocytes at the four genome copy stage may provide the informational redundancy needed to repair damage in the DNA of the germline. [15] The repair process used appears to be homologous recombinational repair [15] [16] Prophase arrested oocytes have a high capability for efficient repair of DNA ...
The species with longer lifespans were found to have slower accumulation of DNA damage, a finding consistent with the DNA damage theory of aging. [119] In healthy humans after age 50, endogenous DNA single- and double-strand breaks increase linearly, and other forms of DNA damage also increase with age in blood mononuclear cells. [ 120 ]