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Updated: Mar 29, 2026

Using Caenorhabditis elegans for Studying Trans- and Multi-Generational Effects of Toxicants
Published on: July 29, 2019
Nanoplastic exposure alters oxidative stress, immunity, and digestive function in Pinctada fucata martensii
Jinyu Qiu1, Fenglan Lu1, Ruijuan Hao2
1Fisheries College, Guangdong Ocean University, Zhanjiang, 524088, China.
Abstract:
This study investigated the effects of nanoplastic (NP) exposure (0.15, 1.5 and 15 mg/L for 60 days) on Pinctada fucata martensii using integrated biochemical and transcriptomic analyses following exposure and a 7-day recovery period. Results showed that NP exposure induced significant oxidative stress, characterized by concentration- and time-dependent suppression of SOD, GPx, and CAT activities, alongside dynamic alterations in MDA content. A transient rebound in antioxidant enzyme activities was observed on day 15, followed by a significant decline by day 60. Concurrently, immunoenzyme (ACP, AKP) and digestive enzyme (amylase, protease) activities were significantly inhibited. A 7-day recovery period mitigated these disturbances in lower concentration groups (0.15 and 1.5 mg/L), but significant effects persisted in the 15 mg/L group. The differentially expressed genes (DEGs) between CG and EGs at 60 days post-exposure were determined by transcriptome data analysis, which identified 212 upregulated and 95 downregulated DEGs. Similarly, 491 downregulated and 577 upregulated DEGs were identified between the EGs and CG at 67 days post-exposure. Functional analysis revealed that exposure to NPs exerted adverse effects on detoxification, immune response, apoptosis, cytoskeletal dynamics, protein synthesis, and homeostasis in P. f. martensii at 60 days post-exposure. Short-term recovery experiments induced the aberrant expression of an increased number of genes, suggesting that NP exposure exerts long-term effects at a molecular level, potentially resulting in the establishment of a new equilibrium in P. f. martensii. These findings indicate that NP exposure causes substantial physiological and molecular dysregulation, with incomplete recovery at high concentrations, elucidating the underlying toxic mechanisms and potential long-term ecological risks.

