Wu Y Y, Tian W F, Cheng C X, Yang L, Ye Q Q, Li W H, Jiang J Y
Key Laboratory of Ecology of Rare and Endangered Species and Environmental Protection, Guangxi Normal University, Ministry of Education, Guilin 541004, China.
College of Biotechnology, Guilin Medical University, Guilin 541004, China.
Ecotoxicol Environ Saf. 2023 Oct 1;264:115416. doi: 10.1016/j.ecoenv.2023.115416. Epub 2023 Aug 28.
Cadmium (Cd) is a common contaminant in aquatic environments. However, little is known about the mechanisms underlying Cd toxicity in the freshwater snail Cipangopaludina cathayensis (Heude, 1890). This study to investigate the toxic effects of Cd on the standard metabolism, antioxidant activities, immune function, and hepatopancreas transcriptome profiles of C. cathayensis. C. cathayensis was exposed to 0.25, 0.5, 1.0, or 1.5 mg/L Cd for 3 h, with results showing that Cd significantly inhibited oxygen consumption and ammonia excretion and disrupted the respiratory metabolism of C. cathayensis. In addition, the O:N ratio dropped below 7, indicating that C. cathayensis may rely exclusively on proteins as an energy source under Cd stress. To understand how Cd impacts the antioxidant activities, immune function, and transcriptional profiles, C. cathayensis were exposed to 0.5 (low exposure, L14) or 1.5 (high exposure, H14) mg/L Cd for 14 days. Our results indicate that Cd exposure leads to oxidative stress and immunosuppression, with the latter effect being larger for exposure to higher Cd concentrations. A total of 2172 differentially expressed genes (DEGs) were identified by transcriptome analysis of the hepatopancreas, of which 885 were upregulated and 1287 were downregulated. Gene ontology and KEGG analyses revealed that the DEGs in the H14 group are enriched for energy generation terms and the "oxidative phosphorylation" pathway, respectively. Therefore, up-regulation of energy metabolism may be an adaptive strategy under Cd stress. Moreover, several genes involved in antioxidant activity were downregulated, whereas genes related to reactive oxygen species generation were upregulated. In addition, many immunity-related genes were identified within the DEGs, indicating that Cd toxicity may affect immune defense. Further, DEGs in the H14 group were enriched for disease-associated pathways. Taken together, our results indicate that Cd exposure leads to metabolic disorders, oxidative stress, and immunosuppression and thus may potentially contribute to disease outbreaks.
镉（Cd）是水生环境中的常见污染物。然而，对于淡水螺蛳中华圆田螺（Cipangopaludina cathayensis，Heude，1890）中镉毒性的潜在机制知之甚少。本研究旨在探究镉对中华圆田螺标准代谢、抗氧化活性、免疫功能及肝胰腺转录组图谱的毒性作用。将中华圆田螺暴露于0.25、0.5、1.0或1.5 mg/L的镉中3小时，结果显示镉显著抑制了氧气消耗和氨排泄，并扰乱了中华圆田螺的呼吸代谢。此外，氧氮比降至7以下，表明中华圆田螺在镉胁迫下可能完全依赖蛋白质作为能量来源。为了解镉如何影响抗氧化活性、免疫功能和转录图谱，将中华圆田螺暴露于0.5（低暴露，L14）或1.5（高暴露，H14）mg/L的镉中14天。我们的结果表明，镉暴露会导致氧化应激和免疫抑制，对于较高镉浓度的暴露，后者的影响更大。通过对肝胰腺的转录组分析，共鉴定出2172个差异表达基因（DEG），其中885个上调，1287个下调。基因本体和KEGG分析表明，H14组中的DEG分别富集于能量产生术语和“氧化磷酸化”途径。因此，能量代谢的上调可能是镉胁迫下的一种适应性策略。此外，几个参与抗氧化活性的基因被下调，而与活性氧产生相关的基因被上调。此外，在DEG中鉴定出许多与免疫相关的基因，表明镉毒性可能影响免疫防御。此外，H14组中的DEG富集于疾病相关途径。综上所述，我们的结果表明，镉暴露会导致代谢紊乱、氧化应激和免疫抑制，因此可能会引发疾病爆发。
