Mitochondrial dysfunction in oocytes: implications for fertility and ageing.

Abstract

The impact of environmental pollution on fertility has become an essential issue in global public health. Maturation, fertilisation, and embryonic development of oocytes depend on the energy provided by mitochondria; however, with increased environmental pollution and ageing, mitochondrial dysfunction and its subsequent functional and metabolic abnormalities have become leading causes of female fertility decline. When mitochondrial dysfunction occurs in the oocyte, reduced metabolic efficiency leads to impaired nuclear and cytoplasmic maturation of the oocyte, affecting the quality of the oocyte, which further contributes to decreased female fertility and increased risk of infertility, miscarriage, and aneuploid foetuses due to ovarian dysfunction. Several factors affect mitochondrial function, including excess reactive oxygen species (ROS)-induced mutations in mitochondrial DNA (mtDNA), changes in mtDNA copy number, oxidative stress (OS), damage to key cellular components and organelles, and changes in metabolic intermediates and byproducts at the cellular level, further affecting oocyte developmental competence. Mitochondrial dysfunction leads to problems such as abnormal spindle formation and chromosome misalignment, reducing fertilisation potential and embryonic developmental capacity. Mitochondrial dysfunction plays a key role in oocyte ageing and the decline in germ cell function, and an in-depth study of its molecular mechanisms and intervention strategies is highly important for slowing oocyte ageing, increasing fertility, and improving the success rate of assisted reproduction techniques. Clinical trial numberNot applicable.