Physio-Transcriptomic Mechanism of Antimony Tin Oxide Nanoparticle-Induced Midgut Toxicity in Bombyx mori

The silkworm (<i>Bombyx mori</i>) is an economically important insect that plays a crucial role in agricultural development. Antimony tin oxide, a high-tech multifunctional nanomaterial, is extensively utilized in contemporary industries due to its properties of transparency, conductivity, and stability. Nevertheless, the toxicity and potential adverse effects of antimony tin oxide on living organisms remain poorly understood. In this study, we evaluated the effects of antimony tin oxide at varying concentrations (0-3.2 μg/μL) on the growth, oxidative stress response, gene expression, and midgut integrity of fifth-instar silkworm larvae. Exposure to high concentrations of antimony tin oxide resulted in a significant reduction in larval weight and severely disrupted the antioxidant defense system. RNA sequencing (RNA-Seq) analysis identified 239 differentially expressed genes (DEGs), which were confirmed by qPCR, revealing up-regulated lipid synthesis gene <i>AGPAT5</i>, down-regulated chitin degradation gene <i>Chi</i>, and suppressed glycerolipid hydrolysis gene <i>H9J6N7_BOMMO</i>. Histopathological and ultrastructural examinations revealed severe damage to the structure of midgut epithelial cells. Structural and functional analysis of conserved domains in key DEG-encoded proteins revealed that gene dysregulation disrupted energy metabolism and compromised the physical barrier, ultimately linking molecular abnormalities to observed tissue damage. These findings elucidate the mechanisms by which antimony tin oxide induces midgut toxicity through interference with critical metabolic pathways and functional perturbations at the molecular level.