Role of Apoptosis in Male Infertility: Therapeutic Targets and Strategies

Apoptosis, or programmed cell death, plays a significant role in spermatogenesis and sperm quality. Environmental factors, xenobiotics, chemicals, stress, diabetes, etc., persuade oxidative stress (OS) and reactive oxygen species (ROS) production, which can induce apoptosis in testicular cells, leading to impaired sperm production and functions and ultimately exacerbating male infertility. Apoptosis markers such as caspase activation, phosphatidyl serine externalization, mitochondrial membrane potential changes, and DNA fragmentation are evident in ejaculated spermatozoa of infertile males. ROS significantly impact male infertility through various signaling pathways. Apoptosis also regulates male germ cells from early embryonic stages through fertilization, maintaining Sertoli to germ cell ratios and ensuring testicular quality control. Understanding the molecular pathways linking apoptosis, OS, excess ROS production, and male infertility is crucial for developing targeted interventions to mitigate reproductive complications in men. This chapter highlights the intricate interplay between apoptosis, OS, and male infertility, emphasizing the need for comprehensive management strategies.