Nano-Zinc Iron Oxide Elicits Oxidative Stress-Driven Midgut Damage and Developmental Suppression in Bombyx mori

The silkworm, Bombyx mori, a key economic insect, has been employed as a model organism to investigate the toxicological effects and underlying mechanisms of zinc iron oxide nanoparticle exposure on its growth and development, midgut tissue structure, and physiological functions. Exposure to zinc iron oxide inhibited larval growth and development, which was accompanied by pathological alterations in the midgut, including a reduction in columnar cells, vacuolation, chromatin condensation, microvilli shedding, and disrupted tight junctions, which directly impaired the intestinal barrier integrity and nutrient absorption. Furthermore, zinc iron oxide exposure resulted in elevated reactive oxygen species levels, decreased superoxide dismutase and glutathione contents, and increased catalase activity, indicating the activation of oxidative stress. This stress-induced mitochondrial response, characterized by the observation of autophagic vesicles, suggests the potential mitophagy of activation in action to zinc iron oxide exposure, thereby preserving cellular homeostasis. This was also associated with the downregulation of most genes involved in purine metabolism, the peroxisome, the biosynthesis of amino acids, the ribosome pathway, and carbon metabolism pathways, leading to reduced protein synthesis and energy supply, ultimately resulting in larval developmental retardation. This study elucidates the intestinal-targeted toxicity of zinc iron oxide nanoparticles in lepidopteran insects, providing direct in vivo experimental evidence for evaluating the ecological risk of zinc iron oxide in sericulture environments. Furthermore, it offers a novel research avenue for developing intestinal intervention strategies aimed at mitigating the toxic effects of nanomaterials and ensuring the stability of economically important traits in silkworms.