Effects of cadmium on intestinal histology and microbiota in freshwater crayfish (Procambarus clarkii).

In this study, Procambarus clarkii (P. clarkii) were exposed to different concentrations (0, 2, 5 and 10 mg/L) of cadmium (Cd). We studied the effects of Cd exposure on intestinal histology and microbiota in P. clarkii. The results demonstrated that exposure to Cd caused histological alterations in the intestines of P. clarkii. Meanwhile, high-throughput sequencing analysis revealed that Cd exposure could alter the richness, diversity, and composition of intestinal microbiota in P. clarkii. At the phylum level, the relative abundances of the prevalent phyla Firmicutes, Proteobacteria, Bacteroidetes, Fusobacteria, and Actinobacteria changed significantly after exposure to Cd. At the genus level, the most prevalent genera with significant difference in relative abundance were Bacteroides, Clostridium XlVb, Hafnia, Buttiauxella, Shewanella, Anaerorhabdus, Alistipes, Arcobacter, Azoarcus, Chryseobacterium, and so on. Furthermore, functional prediction analysis of intestinal microbial communities showed that Cd exposure could significantly alter the pathways related to metabolism, diseases, cellular processes, and so on. Taken together, exposure to Cd could induce intestinal histological damage and affect intestinal microbiota composition and functions of P. clarkii. Our study can be an important step toward a better understanding of the toxic effects of Cd on aquatic crustaceans.

Cadmium-induced oxidative stress, histopathology, and transcriptome changes in the hepatopancreas of freshwater crayfish (Procambarus clarkii).

Cadmium (Cd) is a common contaminant in environment. Crayfish are considered suitable for indicating the impact of heavy metals on the environment. However, there is limited information on the mechanisms causing damage to the hepatopancreas of Procambarus clarkii exposed to Cd. We exposed adult male P. clarkii to 2.0, 5.0, and 10.0 mg/L Cd for 24, 48, and 72 h to explore Cd toxicity. Afterwards, we measured bioaccumulations in the hepatopancreas and determined malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferase (GST). Additionally, the hepatopancreas histopathology was analyzed and the transcriptome analysis of the P. clarkii hepatopancreas under Cd stress was conducted. The results revealed that hepatopancreas could accumulate Cd in a time- and dose-dependent manner. Cd induced significant changes in MDA content and antioxidant enzyme activity. Severe histological alterations were observed in crayfish hepatopancreas. After 72 h exposure to 2.0, 5.0, and 10.0 mg/L Cd, transcriptome analysis identified 1061, 747, and 1086 differentially expressed genes (DEGs), respectively. Exposure to 5.0 mg/L Cd inhibited heme binding, tetrapyrrole binding, iron ion binding and activity of oxidoreductase and sulfotransferase, while exposure to 10.0 mg/L Cd enhanced the export of matters from nucleus. In the hepatopancreas treated with 10.0 mg/L Cd, pathways related to diseases and immune system were significantly enriched. Meanwhile, 31, 31, 24, 7, and 12 identified DEGs were associated with the oxidation-reduction process, immune system, ion homeostasis, digestion and absorption, and ATPases, respectively. Our study provides comprehensive information for exploring the toxic mechanisms of Cd and candidate biomarkers for aquatic Cd risk evaluation.