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

## TL;DR

This study explores how antimony tin oxide nanoparticles harm silkworms, revealing toxic effects on growth and gut health through disrupted metabolism.

## Contribution

The study identifies specific gene dysregulation and metabolic pathways affected by antimony tin oxide in silkworms.

## Key findings

- High concentrations of antimony tin oxide reduced larval weight and damaged midgut cells in silkworms.
- RNA-seq identified 239 dysregulated genes, including upregulated lipid synthesis and downregulated chitin degradation genes.
- Gene dysregulation disrupted energy metabolism and compromised the midgut's physical barrier.

## Abstract

Antimony tin oxide nanomaterials are widely used in industry, but their biological toxicity remains unclear. This study investigated the effect of antimony tin oxide on silkworms (Bombyx mori), an economically important insect, with a focus on larval growth and midgut health. Exposure to high antimony tin oxide concentrations (up to 3.2 μg/μL) significantly reduced larval weight, damaged midgut cell structures, and impaired antioxidant defenses. RNA-seq analysis identified 239 dysregulated genes validated by qPCR, upregulating lipid synthesis (AGPAT5), down-regulating chitin degradation (Chi), and suppressing glycerolipid hydrolysis (H9J6N7_BOMMO). These findings reveal the toxic mechanisms of antimony tin oxide through metabolic interference, highlight potential risks to sericulture, and urge environmental caution in nanomaterial applications.

The silkworm (Bombyx mori) 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 AGPAT5, down-regulated chitin degradation gene Chi, and suppressed glycerolipid hydrolysis gene H9J6N7_BOMMO. 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.