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Oocyte abnormalities can be caused by a variety of genetic factors affecting different stages in meiosis. [1] Moreover, ageing is associated with oocyte abnormalities since higher maternal age is associated with oocytes with a reduced gene expression of spindle assembly checkpoints which are important in maintaining stability in the genome.
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.
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.
In humans and other mammals, DNA damage occurs frequently and DNA repair processes have evolved to compensate. [11] In estimates made for mice, DNA lesions occur on average 25 to 115 times per minute in each cell, or about 36,000 to 160,000 per cell per day. [12] Some DNA damage may remain in any cell despite the action of repair processes.
DNA repair defects are seen in nearly all of the diseases described as accelerated aging disease, in which various tissues, organs or systems of the human body age prematurely. Because the accelerated aging diseases display different aspects of aging, but never every aspect, they are often called segmental progerias by biogerontologists .
Oocytes (female germ cells) located in the primordial follicle of the ovary are in a non-growing prophase arrested state, but are able to undergo highly efficient homologous recombinational repair of DNA damages including double-strand breaks. [8] This capability allows the maintenance of genome integrity and protection of the health of ...
In male germ cells and spermatozoa, and also in female oocytes, special DNA repair mechanism are present that function to maintain the integrity of the genomes that are to be passed on to progeny. [13] These DNA repair pathways include homologous recombinational repair, non-homologous end joining, base excision repair and DNA mismatch repair. [13]
Thus, although the majority of oocytes are produced in female fetuses before birth, these pre-eggs remain arrested in the dictyate stage until puberty commences and the cells complete ootidogenesis. In both mouse and human, oocyte DNA of older individuals has substantially more double-strand breaks than that of younger individuals. [4]