Abstract：
To investigate the impact of chlorantraniliprole on Procambarus clarkii, acute toxicity tests were performed. Results indicated that 96 h post-exposure to chlorantraniliprole (60 mg/L) led to the separation of the hepatopancreas basement membrane, causing cell swelling, rupture, and vacuolation. Moreover, acid phosphatase (ACP) and alkaline phosphatase (AKP) activities exhibited divergent trends across four concentrations of chlorantraniliprole (0, 30, 60, and 90 mg/L). Hydrogen peroxide (H2O2) and catalase (CAT) levels significantly increased, while total superoxide dismutase (T-SOD) and malonaldehyde (MDA) activities decreased, indicating oxidative stress in the hepatopancreas. A total of 276 differentially expressed genes (DEGs) were identified, with 204 up-regulated and 72 down-regulated. Out of these, 114 DEGs were successfully annotated and classified into 99 pathways, with a primary focus on the cytochrome P450-mediated xenobiotic metabolism pathway. The DEGs enriched in this pathway, along with transcriptome data, were validated using quantitative-polymerase chain reaction. This study enhances the transcriptome database of P. clarkii and provides fundamental insights into its immune defense and antioxidant mechanisms. Additionally, it lays a theoretical foundation for future research on disease prevention in P. clarkii within rice-shrimp culture systems.
摘要：
为了研究氯苯三虫对克氏原虫的影响，进行了急性毒性试验.结果表明，暴露于chloantraniliprole（60mg/L）后96小时导致肝胰腺基底膜分离，导致细胞肿胀,破裂,和空泡。此外，酸性磷酸酶（ACP）和碱性磷酸酶（AKP）活性在四种浓度（0、30、60和90mg/L）的chloantraniliprole中表现出不同的趋势。过氧化氢（H2O2）和过氧化氢酶（CAT）水平显著升高，总超氧化物歧化酶(T-SOD)和丙二醛(MDA)活性降低,表明肝胰腺中的氧化应激。共鉴定出276个差异表达基因(DEGs),204上调，72下调。在这些中，114个DEGs被成功注释并分类为99个途径，主要集中在细胞色素P450介导的外源性生物代谢途径。DEGs在这个途径中富集,连同转录组数据，使用定量聚合酶链反应进行了验证。这项研究增强了克氏疟原虫的转录组数据库，并提供了对其免疫防御和抗氧化机制的基本见解。此外,为今后在稻虾养殖体系内开展克氏疟原虫疾病预防研究奠定了理论基础。
