Lead (Pb²⁺) is a persistent environmental toxicant that adversely affects male and female reproductive health through endocrine disruption, oxidative stress, inflammation, mitochondrial dysfunction, DNA damage, apoptosis, and epigenetic alterations. Pb²⁺ disrupts the hypothalamic-pituitary-gonadal and hypothalamic-pituitary-ovarian axes while directly damaging reproductive cells. Excessive ROS generation, impaired antioxidant defense, and dysregulation of Nrf2 and NF-κB signaling promote oxidative and inflammatory injury, while mitochondrial dysfunction and impaired autophagy further accelerate cellular damage. In males, Pb²⁺ impairs Leydig and Sertoli cell function, steroidogenesis, blood-testis barrier integrity, spermatogenesis, sperm maturation, and fertilization, resulting in reduced sperm quality, motility, and DNA integrity. In females, Pb²⁺ disrupts ovarian steroidogenesis, follicular development, oocyte quality, and ovarian reserve, contributing to menstrual irregularities, impaired ovulation, subfertility, and adverse pregnancy outcomes. Epigenetic alterations may further contribute to persistent reproductive dysfunction and potentially affect offspring's health. Current management primarily involves exposure reduction and clinically indicated chelation, while antioxidant and micronutrient interventions may provide supportive protection. However, limitations in human evidence and incomplete understanding of molecular interactions remain important challenges. Integrating multi-omics approaches with reproductive phenotyping in the future may facilitate biomarker discovery and targeted therapy. Overall, Pb²⁺-induced reproductive toxicity is a multifactorial molecular disorder, emphasizing the need for early detection, preventive strategies, and targeted interventions to protect reproductive health.