ORIGINAL ABSTRACT

Glyphosate, the active ingredient in many herbicides, has been extensively used in agricultural practices worldwide, leading to environmental persistence of the herbicide and its main metabolite, aminomethylphosphonic acid (AMPA), particularly in water and soil. Despite a short half-life in biological fluids, frequent detection of glyphosate and AMPA in urine samples suggests ongoing human exposure. Evidence indicates that glyphosate and AMPA may exert endocrine-disrupting effects on testicular function. Glyphosate exposure may disrupt the hypothalamic-pituitary-gonadal axis, impacting serum testosterone levels and other key hormones involved in spermatogenesis and fertility. It has also been shown to impair key cellular processes within the male reproductive system, including oxidative stress, mitochondrial dysfunction, and hormone biosynthesis. These findings raise concerns about the herbicide's ability to compromise sperm production, structure, and motility, which are crucial factors for male fertility. This review examines the mechanisms underlying glyphosate-induced testicular toxicity, emphasizing endocrine disruption, oxidative stress, and mitochondrial dysfunction, and highlights the need for further studies on long-term effects across different life stages and genetic backgrounds. Glyphosate-induced testicular toxicity can be counteracted by antioxidant agents, which emerge as promising therapeutic strategies in need of further investigation.