Nanoplastic exposure induces exoskeletal misdevelopment in juvenile Tachypleus tridentatus: Compensatory hardening versus molecular suppression

Microplastic and nanoplastic pollution poses a significant threat to marine ecosystems, yet its impact on the critical physiological processes of endangered marine arthropods remains poorly understood. This study reveals that chronic exposure to polystyrene nanoplastics (1, 10, 100 μg/L) disrupts the exoskeletal sclerotization process in first-instar juveniles of the endangered Chinese horseshoe crab, Tachypleus tridentatus. Our results demonstrate that nanoplastics trigger a compensatory hardening response in the juvenile carapace, which depends on both the exposure dose and duration. This response manifested as a larger and biomechanically stronger shell, with increased maximum load and tensile strength. Despite this enhanced physical strength, we observed a significant suppression of key sclerotization-related genes (E74, Calmodulin, and Carbonic Anhydrase). This gene downregulation suggests that the normal pathways for molting and shell mineralization were being disrupted. Conversely, a significant elevation in N-acetyl-β-D-glucosaminidase (NAG) activity suggested a disrupted balance between exoskeleton degradation and synthesis. In conclusion, nanoplastic exposure causes a profound mismatch between gene expression and phenotypic outcomes in T. tridentatus, forcing a potentially costly compensatory response that may impair their molting success and long-term survival, thereby highlighting a severe ecological risk to this ancient species.