Carbamate insecticide bendiocarb induces complex embryotoxic effects, including morphological, behavioral, transcriptional, and immunological alterations in zebrafish.

The emergence and spread of vector-borne diseases necessitate the increased use of insecticides, such as carbamates, raising concerns about their potential toxicological risks to non-target organisms, including humans. Bendiocarb, frequently applied in indoor spraying operations and detected in maternal and fetal circulation, warrants particular attention for its developmental toxicity. This study aimed to assess transcriptional and phenotypic effects of sublethal bendiocarb exposure at concentrations of 0.035, 0.2, 0.4, 0.75, and 1.5 mg/L, using zebrafish embryos, a vertebrate model for developmental toxicity testing. Our analyses revealed acetylcholinesterase inhibition-associated morphological and behavioral abnormalities, including reduced locomotor activity in response to both visual and tactile stimuli, as well as impaired non-associative learning. Transcriptomic analysis indicated activation of muscle, immune, and metabolic pathways, while neurodevelopmental, phototransduction, and cell proliferation processes were suppressed. Consistent with these molecular findings, structural damage was observed in the retina, skeletal muscle, and notochord. Furthermore, bendiocarb exposure disrupted neutrophil granulocyte distribution and impaired inflammatory responses. Altogether, our results provide new insights into the embryotoxic effects of bendiocarb, highlighting its potential to disrupt early vertebrate development. These findings provide mechanistic insight that may support more informed evaluations of potential public health risks associated with developmental exposure to carbamates.