Chronic exposure to glufosinate-ammonium induces male reproductive toxicity by mitochondrial impairment and spermatogenesis disruption in zebrafish (Danio rerio).

Glufosinate-ammonium (GLA) is one of the widely used organophosphorus herbicides. Although increasing evidence indicates that the GLA is reproductively toxic to lizards and mammals, knowledges about the long-term effects of GLA on organisms are still limited. In this study, zebrafish (Danio rerio) embryos were exposed to varying concentrations of GLA (0 μg/L, 15 μg/L, 300 μg/L and 6000 μg/L) for 120 days to assess the reproductive toxicity of GLA in male zebrafish and its potential mechanisms. GLA exhibited significant reproductive toxicity, evidenced by delayed testis maturation, reduced sperm density and impaired sperm motility in male zebrafish. Furtherly, GLA triggered oxidative stress by excessive ROS production and lipid peroxidation, leading to cell apoptosis via both mitochondrial and extrinsic death receptor pathways at environmentally relevant concentrations (15 μg/L). Notably, GLA disrupted the mitochondrial structure, impaired mitochondrial membrane potential and decreased ATP content. Additionally, GLA at higher concentrations exhibited estrogenic activity via increasing vitellogenin (VTG) contents in the liver and the plasma estradiol/testosteone (E2/T) ratios in males. Our study demonstrates that long-term GLA exposure induces reproductive dysfunction in male zebrafish, primarily mediated through mitochondrial impairment-induced oxidative stress in the testes. Furthermore, we provide robust evidence for the estrogenic effects of GLA at higher concentrations.