Using transgenic zebrafish to assess the effects of SCCPs exposure on embryonic neural development and its potential mechanisms.

Short-chain chlorinated paraffins (SCCPs), categorized as persistent organic pollutants, raise substantial concerns regarding their potential neurodevelopmental toxicity. This study utilized transgenic zebrafish models to examine SCCPs-induced developmental neurotoxicity. Embryos exposed to SCCPs (0-200 μg/L) displayed no significant impact on mortality or hatching rates, yet exhibited dose-dependent teratogenic effects such as pericardial edema. Crucially, confocal imaging revealed pronounced neural impairments, characterized by reduced intersegmental neural cells and aberrant synaptic projections in motor neurons. TUNEL and BrdU staining indicated increased apoptosis and suppressed proliferation within the dorsal spinal cord. Molecular analysis indicated upregulation of key apoptosis- and autophagy-related genes, alongside altered expression of neural markers. RNA sequencing identified 104 differentially expressed genes and verified snap25b as a pivotal hub gene. Collectively, these results provide novel integrated evidence showing associations between SCCP exposure and abnormal apoptosis, inhibited cell proliferation, as well as disrupted neural circuit formation. Combined with transgenic zebrafish lines, transcriptomic profiling and imaging approaches, our findings suggest that SCCP exposure is linked to abnormal neurodevelopment, highlighting significant environmental health risks.