<p>Dimefluthrin is a widely used insecticide that exhibits toxicity to numerous aquatic organisms. However, its developmental effects on fish remain poorly understood. This study investigated the impact of dimefluthrin exposure on zebrafish (<i>Danio rerio</i>) development. Embryos were exposed to 0.2, 0.6, and 0.8 µM dimefluthrin for 96&#xa0;h post-fertilization (hpf). Morphological alterations, oxidative stress levels, and the transcription of embryogenesis-related marker genes were assessed. Dimefluthrin exposure induced significant locomotor impairments, characterized by intensified spastic movements and altered swimming trajectories in larvae. Swim bladder formation was inhibited, leading to non-inflated swim bladders. Notably, dimefluthrin exposure resulted in a 43.33% increase in superoxide dismutase (SOD) enzymatic activity and an 82.25% decrease in malondialdehyde (MDA) content compared to controls. Furthermore, dimefluthrin disrupted the expression of dopamine-related genes (<i>th</i> and <i>slc6a3</i>) and swim bladder marker genes (<i>anxa5b</i> and <i>hprt1l</i>). These findings demonstrated that dimefluthrin induces locomotor dysfunction, oxidative stress, and swim bladder non-inflation in zebrafish, providing valuable insights into its potential environmental risk assessment.</p>