Disruption of intestinal structure, tight junction complex, immune response and microbiota after chronic exposure to copper in swamp eel (Monopterus albus).

As an essential micronutrient, copper is crucial in aquatic organisms' growth and development. Numerous studies have consistently reported that excessive intake of copper can have harmful effects on organisms. However, there are limited studies on the impact of copper on the intestine of the swamp eel (Monopterus albus). This study aimed to investigate the changes of intestinal histopathology, tight junction complex, immune response, and microbiota in swamp eel treated with 0 mg/L Cu2+, 0.05 mg/L Cu2+, and 0.10 mg/L Cu2+ for 56 d. Intestinal histopathology showed major changes such as the increased number of erythrocytes and goblet cells in the lamina propria, and separation of the lamina propria. The expression of genes involved in tight junction complex (ZO-1, Claudin-3, Claudin-12 and Claudin-15) was significantly changed. In addition, copper exposure significantly increased the mRNA levels of TLR3, TLR7, TLR8, NF-κB, I-κB, TNF-α and IL-8, especially in 0.10 mg/L Cu2+ group. In contrast, the relative expression level of anti-inflammatory cytokine TGF-ß was significantly decreased after exposure to copper. Analysis of the intestinal microbiome showed the intestinal microbiota of swamp eels in the control and copper exposure groups were dominated by Firmicutes and Proteobacteria at the phylum level. Notably, copper exposure changed the diversity of the intestinal microbiota and decreased the relative abundance of Firmicutes and Proteobacteria in the intestine of swamp eel. Collectively, this study demonstrates that chronic copper exposure induces intestinal pathologic changes and inflammatory response, disrupts the intestinal microbial diversity and microbiota composition, and decreases intestinal barrier function in swamp eel, which enhances our understanding of copper-induced intestinal toxicity in fish.

Combined transcriptomics and metabolomics analysis reveals lipid metabolic disruption in swamp eel (Monopterus albus) under chronic waterborne copper exposure.

Excessive copper can induce many adverse effects although it's an essential trace element in organisms. The effects of copper on the lipid metabolism have aroused increasing attention. This study investigated the liver lipid metabolism in swamp eel (Monopterus albus, M. albus) chronically exposed to 0, 10, 50, and 100 µg/L Cu2+ for 56 days. The results showed that copper increased the contents of triglyceride (TG), total cholesterol (T-CHO), non-esterified fatty acids (NEFA), and lipid droplets. Transcriptomic analysis found 1901 differentially expressed genes (DEGs) and 140 differential alternative splicing (DAS) genes in the 50 µg/L Cu2+ group, and 1787 DEGs and 184 DAS genes in the 100 µg/L Cu2+ group, respectively, which were enriched in peroxisome proliferator-activated receptor (PPAR), adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK), and other signaling pathways. The expression levels of key genes related to PPAR and AMPK signaling pathways were significantly down-regulated after chronic exposure to Cu2+. Meanwhile, metabolomics analysis showed that 52 and 110 differentially expressed metabolites (DEMs) were identified, which were mainly enriched in glycerophospholipids metabolism and steroid synthesis. Moreover, combined analysis of transcriptome and metabolome showed that glycerophospholipid metabolism co-enriched 19 down-regulated DEGs and 4 down-regulated DEMs. Taken together, our results suggested that chronic waterborne copper exposure promoted lipid synthesis, disrupted the metabolic homeostasis of glycerophospholipid, and led to excessive hepatic lipid deposition in M. albus. The combined omics approach enhanced our understanding of copper pollution to lipid metabolism.

Histological alterations, oxidative stress, and inflammatory response in the liver of swamp eel (Monopterus albus) acutely exposed to copper.

Copper (Cu) is widely used as an essential trace element in diets as well as a therapeutic chemical. However, excessive Cu has deleterious effects on organisms, including teleosts. Although numerous toxic effects of Cu have been reported, the effects of Cu exposure on the swamp eel (Monopterus albus) as well as the underlying mechanisms have not yet been elucidated. In this study, swamp eels were acutely exposed to 100, 200, and 400 µg/L of Cu for 96 h to evaluate liver histopathology, oxidative stress, and inflammation. Dissolution of hepatocyte membrane, vacuolar degeneration, and inflammatory cell infiltration were detected in the livers of the Cu-treated swamp eels, especially in the 400 µg Cu/L group. Cu-induced hepatic dysfunction was further verified by the elevated activities of glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT) and transcript levels of GOT and GPT genes. In addition, Cu exposure decreased the activities of total superoxide dismutase T-SOD and catalase (CAT) and the contents of glutathione (GSH) and total antioxidant capacity (T-AOC) and increased the levels of malondialdehyde (MDA). Cu exposure also significantly decreased the transcript levels of glutathione synthetase (GSS) and increased the transcript levels of SOD1, SOD2, CAT, and heme oxygenase-1 (HO-1) genes. Furthermore, pro-inflammatory genes such as interleukin (IL)-1ß, tumor necrosis factor-α (TNF-α), and IL-8 were significantly upregulated. These results indicate that Cu induces oxidative stress and inflammatory response and causes pathological changes in the liver of the swamp eel.

Effects of MC-LR on histological structure and cell apoptosis in the kidney of grass carp (Ctenopharyngodon idella).

Microcystin-LR (MC-LR) is a well-known hepatotoxin; however, increasing evidence suggests that it might induce kidney injury. Grass carp (Ctenopharyngodon idella) is one of the most important farmed species and may be affected by MC-LR releasing into waterbody during cyanobacterial bloom. Here, this present study aimed to explore the nephrotoxicity of grass carp by MC-LR. The grass carp received a single intraperitoneal injection of different doses of MC-LR (0, 25, 75, and 100 µg/kg body weight (BW)), and the kidneys were isolated at 24 and 96 h post-injection (hpi). Histopathological examination revealed kidney lesions, with severe hemorrhage, necrosis of the interstitium, and dilation of Bowman's capsule in the 75 and 100 µg MC-LR/kg BW groups. Under transmission electron microscopy, a larger number of swelling and vacuolated degeneration of mitochondria were observed; moreover, apoptotic features, such as condensed chromatin and shrinkage of cells, were observed in the 75 and 100 µg MC-LR/kg BW groups at 96 hpi. MC-LR significantly upregulated the number of apoptotic cells in the 75 and 100 µg/kg BW groups at 96 hpi as indicated by terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) assay (P < 0. 05). The results of quantitative assays showed that the mRNA expression of Bax, caspase-9, and caspase-3 in grass carp kidney were significantly increased at 96 hpi in the 75 and 100 µg MC-LR/kg BW groups compared with that in the control group, but Bcl-2 mRNA expression was significantly decreased in all the treatment groups at 24 and 96 hpi. Taken together, these results indicated that MC-LR damaged the kidney structure and resulted in renal apoptosis which may occur via the mitochondrial pathway.