Abstract
The reduction of female fertility over time is considered as a natural consequence of ovarian aging. The exact mechanism underlying this process is not fully elucidated. However, it is becoming increasingly evident that qualitative and quantitative mitochondrial genome alterations might play a relevant role. The former include mitochondrial DNA (mtDNA) damage caused by oxidative stress, the accumulation of acquired mtDNA mutations, the effects of inherited mtDNA mutations, and alterations in the mitochondrial stress response mechanism. The latter refer to alterations in the oocytes, granuolosa cells, and embryonic cells mtDNA content. The present review aims to investigate the evidence about: (1) the effect of qualitative and quantitative mtDNA alterations on female fertility, paying particular attention to those with a pathophysiology characterized by a relevant role of oxidative stress; (2) the use of oocytes, granulosa cells (GCs), embryonic cells, and peripheral blood cells mtDNA copy number as a female fertility surrogate biomarker; (3) experimental therapies tested to try to subvert the ovarian aging process with particular reference to antioxidant treatments.
Highlights
Women attain the peak of fertility in their early and mid-20s
The present review aims to synthesize the evidence about: (1) the effect of qualitative and quantitative Mitochondrial DNA (mtDNA) alterations on female fertility, paying particular attention to those with a pathophysiology characterized by a relevant role of oxidative stress; (2) the use of oocytes, granulosa cells (GCs), embryonic cells and peripheral blood cells mtDNA content as a female fertility surrogate biomarker; (3) experimental therapies tested to try to subvert the ovarian aging process with particular reference to antioxidant treatments
In older women, the GCs in primordial follicles and, as a consequence, the oocytes have been under the effect of low amounts of reactive oxygen species (ROS) derived from the process of mitochondrial respiration for a long time, and probably suffered damage to their mitochondria and mtDNA [31]
Summary
Women attain the peak of fertility in their early and mid-20s. After that, fecundity starts to decline gradually. One may observe a reduced mtDNA content in blastocyst stage embryonic cells when compared to that in oocytes It follows that, in the period of time elapsing from fertilization to implantation, the embryo depends on the function of existing mitochondria [10,11,12]. The present review aims to synthesize the evidence about: (1) the effect of qualitative and quantitative mtDNA alterations on female fertility, paying particular attention to those with a pathophysiology characterized by a relevant role of oxidative stress; (2) the use of oocytes, GCs, embryonic cells and peripheral blood cells mtDNA content as a female fertility surrogate biomarker; (3) experimental therapies tested to try to subvert the ovarian aging process with particular reference to antioxidant treatments. After a full review of titles, abstracts and, in case of doubt, of full texts, a total of 65 studies were included in the qualitative synthesis
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