Submicron silica particles disrupt planarian homeostasis: bridging bioaccumulation, oxidative stress, and growth–regeneration trade-offs

Abstract

Silicosis is a systemic disease caused by prolonged inhalation of free silica dust. Currently, the criteria for evaluating silica toxicity remain rooted in the established fact that spherical particles below 10 μm in diameter can directly penetrate deep lung regions, ultimately leading to pulmonary dysfunction. This functional impairment represents complex pathological alterations, though its potential association with diminished regenerative capacity in lung tissues remains undetermined. Using the classical planarian regeneration model, this study systematically elucidates the size-dependent toxicological effects of silica particles on planarian regeneration, reproduction, and growth, along with their underlying mechanisms. Experimental data demonstrate an inverse correlation between the particle size and inhibitory potency on these biological processes. Bio-transmission electron microscopy analyses revealed preferential accumulation of smaller particles in digestive gland regions, inducing glandular morphological abnormalities and quantitative reduction, accompanied by compromised integrity of epidermal and muscular layers. RNA-seq further delineated the mechanistic basis of silica toxicity. Key findings establish that the size-dependent toxicity of silica particles is correlated with their bioaccumulation efficiency, oxidative stress induction, and disruption of key metabolic pathways. This research provides critical theoretical foundations for nanoparticle ecotoxicological assessments, while highlighting the necessity for reassessing potential health risks associated with submicron silica particles in food and industrial applications.