273METAL-INDUCED MITOCHONDRIAL DYSFUNCTION IN TESTICULAR TOXICITY: MOLECULAR MECHANISMS, THERAPEUTIC STRATEGIES, AND FUTURE PERSPECTIVESHeavy metal contamination has emerged as a major environmental and public health concern, with growing evidence linking arsenic, cadmium, and lead exposure to male reproductive dysfunction. Among the cellular targets of these toxicants, mitochondria play a pivotal role because they regulate ATP production, redox homeostasis, steroidogenesis, calcium signaling, and apoptosis in testicular cells. Disruption of mitochondrial function impairs spermatogenesis, testosterone biosynthesis, and sperm quality, ultimately contributing to male infertility. This review summarizes current advances in the molecular mechanisms underlying metal-induced mitochondrial dysfunction in the testis, with particular emphasis on oxidative stress, mitochondrial DNA damage, electron transport chain inhibition, mitochondrial membrane depolarization, calcium dysregulation, impaired mitophagy, altered mitochondrial dynamics, and activation of intrinsic apoptotic pathways. The review also discusses the consequences of mixed-metal exposure, developmental susceptibility, environmentally relevant lowdose exposure, sex-related considerations, and the need for longitudinal studies to improve translational relevance. In addition, current and emerging therapeutic approaches, including chelation therapy, antioxidants, mitochondria-targeted compounds, modulators of mitochondrial quality control, nanomedicine, and lifestyle interventions, are critically evaluated. A better understanding of mitochondrial mechanisms will facilitate the development of targeted therapeutic strategies and biomarkers for the prevention and treatment of heavy metal-induced male reproductive toxicity.-Research1622026Arsenic; Cadmium; Lead; Testis; Mitochondrial dysfunction; Oxidative stress.Pavitra BehraUttham Memorial College, Raigarh, C.G. 496100 India