Polystyrene Microplastics Impair Intestinal Homeostasis in Juvenile Tachypleus tridentatus Through Oxidative Imbalance and Gut Microbiota Dysregulation

Microplastics (MPs) are ubiquitous marine pollutants that pose increasing ecological risks, yet their effects on intestinal physiology and gut microbial homeostasis during the juvenile developmental stages of Tachypleus tridentatus remain unclear. In this study, fifth- and sixth-instar juveniles of T. tridentatus were exposed to environmentally relevant concentrations of 6.0 μm polystyrene microplastics (PS-MPs; 0, 102, and 104 particles/L) for 7 and 21 days to investigate intestinal physiological responses and potential mechanisms associated with PS-MP exposure. Intestinal retention, oxidative stress, innate immune responses, and gut microbiota were comprehensively evaluated. PS-MP exposure induced concentration-dependent and time-dependent alterations in superoxide dismutase, catalase, malondialdehyde, and lysozyme, suggesting oxidative imbalance and modulation of innate immune responses. Fifth-instar juveniles displayed more pronounced oxidative-stress alterations and divergent innate-immune profiles relative to sixth-instar conspecifics, pointing to greater physiological susceptibility at earlier developmental stages. Gut microbiota analysis revealed pronounced dysbiosis, characterized by a reduced relative abundance of Bacillota, enrichment of Pseudomonadota, depletion of beneficial taxa (e.g., Lactococcus), and increased abundance of opportunistic bacteria, including Pseudomonas and members of Enterobacteriaceae. These physiological and microbial alterations collectively suggest that environmentally relevant PS-MPs impair intestinal homeostasis in juvenile T. tridentatus by inducing oxidative imbalance, modifying innate immune responses, and reshaping gut microbial communities, with clear instar- and exposure time-dependent effects. These findings highlight the importance of considering developmental stages in ecological risk assessment for benthic arthropods.