This article explores the impact of reactive oxygen species (ROS) and mitochondrial dysfunction on reproductive aging. Mitochondria, essential for energy production, generate ROS as a byproduct of oxidative phosphorylation. Excessive ROS levels, linked to mitochondrial dysfunction, contribute to reproductive aging by damaging mitochondrial DNA and impairing cellular functions. ROS also disrupt physiological and pathological pathways in gametes and reproductive tissues, affecting oocyte and sperm quality, fertility, and overall reproductive health. Mitochondria are dynamic organelles with a complex structure, including the outer and inner membranes, and play a critical role in energy metabolism, signal transduction, and cellular homeostasis. ROS production is a key factor in mitochondrial dysfunction, leading to oxidative damage, telomere shortening, and impaired gamete development. The balance between ROS production and antioxidant defenses is crucial for maintaining reproductive health. Excessive ROS levels negatively affect oocyte quality and female fertility by causing oxidative damage to cellular components, leading to reduced oocyte viability and impaired meiotic processes. Similarly, in males, elevated ROS levels can impair sperm motility, viability, and fertility. Mitochondrial dysfunction in sperm can also lead to reduced energy supply, affecting sperm function and fertilization. Mitochondrial dynamics, including fusion and fission, are essential for maintaining mitochondrial function and energy production. Disruptions in these processes can lead to impaired mitochondrial function, affecting oocyte maturation and embryo development. The number and quality of mitochondria in oocytes are critical for reproductive aging, with reduced mtDNA levels and mitochondrial dysfunction contributing to decreased oocyte quality and fertility. Paternal mitochondria can also influence offspring development, as mitochondrial DNA from sperm may be transmitted to offspring. However, the mechanisms of paternal mitochondrial elimination remain unclear. Strategies to mitigate oxidative damage and enhance mitochondrial function, such as antioxidant therapies and mitochondrial transplantation, show promise in improving reproductive health and delaying aging. Understanding the complex interplay between ROS, mitochondrial function, and reproductive aging is essential for developing therapeutic strategies to improve fertility and reproductive health. Future research should focus on elucidating the molecular mechanisms underlying reproductive aging and exploring novel approaches to enhance gamete quality and fertility.This article explores the impact of reactive oxygen species (ROS) and mitochondrial dysfunction on reproductive aging. Mitochondria, essential for energy production, generate ROS as a byproduct of oxidative phosphorylation. Excessive ROS levels, linked to mitochondrial dysfunction, contribute to reproductive aging by damaging mitochondrial DNA and impairing cellular functions. ROS also disrupt physiological and pathological pathways in gametes and reproductive tissues, affecting oocyte and sperm quality, fertility, and overall reproductive health. Mitochondria are dynamic organelles with a complex structure, including the outer and inner membranes, and play a critical role in energy metabolism, signal transduction, and cellular homeostasis. ROS production is a key factor in mitochondrial dysfunction, leading to oxidative damage, telomere shortening, and impaired gamete development. The balance between ROS production and antioxidant defenses is crucial for maintaining reproductive health. Excessive ROS levels negatively affect oocyte quality and female fertility by causing oxidative damage to cellular components, leading to reduced oocyte viability and impaired meiotic processes. Similarly, in males, elevated ROS levels can impair sperm motility, viability, and fertility. Mitochondrial dysfunction in sperm can also lead to reduced energy supply, affecting sperm function and fertilization. Mitochondrial dynamics, including fusion and fission, are essential for maintaining mitochondrial function and energy production. Disruptions in these processes can lead to impaired mitochondrial function, affecting oocyte maturation and embryo development. The number and quality of mitochondria in oocytes are critical for reproductive aging, with reduced mtDNA levels and mitochondrial dysfunction contributing to decreased oocyte quality and fertility. Paternal mitochondria can also influence offspring development, as mitochondrial DNA from sperm may be transmitted to offspring. However, the mechanisms of paternal mitochondrial elimination remain unclear. Strategies to mitigate oxidative damage and enhance mitochondrial function, such as antioxidant therapies and mitochondrial transplantation, show promise in improving reproductive health and delaying aging. Understanding the complex interplay between ROS, mitochondrial function, and reproductive aging is essential for developing therapeutic strategies to improve fertility and reproductive health. Future research should focus on elucidating the molecular mechanisms underlying reproductive aging and exploring novel approaches to enhance gamete quality and fertility.