Abstract
DNA damage is one of the most common threats to meiotic cells. It has the potential to induce infertility and genetic abnormalities that may be passed to the embryo. Here, we reviewed exogenous factors which could induce DNA damage. Specially, we addressed the different effects of DNA damage on mouse oocytes and embryonic development. Complex DNA damage, double- strand breaks, represents a more difficult repair process and involves various repair pathways. Understanding the mechanisms involved in DNA damage responses may improve therapeutic strategies for ovarian cancer and fertility preservation.
Highlights
Increasing attention is being paid to how DNA damage influences mammalian oocytes
In 19 European countries where all clinics report to the assisted reproductive technology register, a total of 350143 assisted reproductive cycles were performed in a population of 370 million, representing 947 cycles per million inhabitants [1]
Complex DNA damage, DNA double-strand breaks (DSBs), represent a more difficult process with various repair pathways, which are the major focus of this review
Summary
Increasing attention is being paid to how DNA damage influences mammalian oocytes. Women undergoing chemotherapy have an increased expectation of fertility preservation. Simple forms of DNA damage such as single-site base damage or singlestrand breaks (SSBs) will be repaired rapidly and [4]. Complex DNA damage, DNA double-strand breaks (DSBs), represent a more difficult process with various repair pathways, which are the major focus of this review. DSBs can be induced by many exogenous or endogenous factors. Γ-H2AX is often used as a marker for DNA DSBs damage, because H2AX becomes phosphorylated within 1–3 min after DSBs and forms foci to recruit repairing factors at break sites [16,17]. The effect of DNA damage caused by endogenous factors resembles programmed DSBs of pachytene. It is repaired by homologous recombination (HR) when. We focused on the DNA damage caused by exogenous factors
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