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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.
When there is DNA damage, Mdm2 is phosphorylated, most likely caused by ATM. The phosphorylation of Mdm2 leads to a reduction in the activity of Mdm2, thus preventing the degradation of p53. Normal, undamaged cell, usually has low levels of p53 while cells under stress and DNA damage, will have high levels of p53. [13]
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.
These reactive chemical species can reach DNA by diffusion and the bimolecular reaction damages the DNA (oxidative stress). Unlike direct DNA damage which causes sunburn, indirect DNA damage does not result in any warning signal or pain in the human body. The bimolecular reactions that cause the indirect DNA damage are illustrated in the figure:
Arrested oocytes do not enter the subsequent stage, anaphase I. DNA double strand breaks, UVB and ionizing radiation induced DNA damage cause an effective block to anaphase promoting complex activity. [57] This checkpoint may help prevent oocytes with damaged DNA from progressing to become fertilizable mature eggs. [57]
Sperm entry causes calcium release into the oocyte. In mammals, this is caused by the introduction of phospholipase C isoform zeta (PLCζ) from the sperm cytoplasm. [1] Activation of the ovum includes the following events: Cortical reaction to block against other sperm cells; Activation of egg metabolism; Reactivation of meiosis; DNA synthesis
Replication stress is induced from various endogenous and exogenous stresses, which are regularly introduced to the genome. [10] These stresses include, but are not limited to, DNA damage, excessive compacting of chromatin (preventing replisome access), over-expression of oncogenes, [11] or difficult-to-replicate genome structures.
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.