<p>The chemical contamination of aquatic ecosystems by commonly used compounds represents a silent yet escalating threat to biodiversity and environmental health. Among these, triclosan (TCS), an antimicrobial agent widely found in personal care products, has emerged as a persistent pollutant that can accumulate in water bodies and disrupt essential biological processes. This study comprehensively evaluated the embryonic developmental toxicity of TCS in zebrafish (<i>Danio rerio</i>), with particular focus on reactive oxygen species (ROS) generation and the modulation of organogenesis-related signaling pathways. After 96&#xa0;h of exposure, TCS induced marked morphological abnormalities during critical stages of embryogenesis, including delayed hatching, hypopigmentation, and pericardial edema. These effects corresponded to a median lethal concentration (LC₅₀) of 363&#xa0;µg/L and a median effective concentration for malformations (EC₅₀) of 309&#xa0;µg/L. Moreover, a marked overproduction of ROS was observed, accompanied by activation of antioxidant enzymes (SOD and CAT) and a significant increase (<i>p</i> &lt; 0.05) in oxidative damage biomarkers (HPO, LPX, PCC). Concurrently, key genes associated with apoptosis (<i>apaf1</i>), ion transport (<i>slc12a1</i>, <i>kcnj1a.1</i>), and embryonic development (<i>tbx2a</i>, <i>tbx2b</i>) were significantly overexpressed (<i>p</i> &lt; 0.05). These findings demonstrate that TCS interferes with fundamental processes of organogenesis through oxidative stress-mediated mechanisms, even at concentrations below current regulatory limits. These findings provide strong evidence for the urgent need to establish stricter limits for the release and environmental monitoring of TCS to safeguard vulnerable aquatic ecosystems.</p>