Mechanisms insights into bisphenol S-induced oxidative stress, lipid metabolism disruption, and autophagy dysfunction in freshwater crayfish.

Bisphenol S (BPS) is widely used in plastic products, food packaging, electronic products, and other applications. In recent years, BPS emissions have increasingly impacted aquatic ecosystems. The effects of BPS exposure on aquatic animal health have been documented; however, our understanding of its toxicology remains limited. This study aimed to explore the mechanisms of lipid metabolism disorders, oxidative stress, and autophagy dysfunction induced in freshwater crayfish (Procambarus clarkii) by exposure to different concentrations of BPS (0 µg/L, 1 µg/L, 10 µg/L, and 100 µg/L) over 14 d. The results indicated that BPS exposure led to oxidative stress by inducing elevated levels of reactive oxygen species (ROS) and inhibiting the activity of antioxidant-related enzymes. Additionally, BPS exposure led to increased lipid content in the serum and hepatopancreas, which was associated with elevated lipid-related enzyme activity and increased expression of related genes. Furthermore, BPS exposure decreased levels of phosphatidylcholine (PC) and phosphatidylinositol (PI), disrupted glycerophospholipid (GPI) metabolism, and caused lipid deposition in the hepatopancreatic. These phenomena may have occurred because BPS exposure reduced the transport of fatty acids and led to hepatopancreatic lipid deposition by inhibiting the transport and synthesis of PC and PI in the hepatopancreas, thereby inhibiting the PI3K-AMPK pathway. In conclusion, BPS exposure induced oxidative stress, promoted lipid accumulation, and led to autophagy dysfunction in the hepatopancreas of freshwater crayfish. Collectively, our findings provide the first evidence that environmentally relevant levels of BPS exposure can induce hepatopancreatic lipid deposition through multiple pathways, raising concerns about the potential population-level harm of BPS and other bisphenol analogues.

Sulforaphane modulates some stress parameters in TPT-exposed Cyprinus carpio in relation to liver metabolome.

This study aimed to investigate the protective effect of sulforaphane (SFN) on liver injury induced by triphenyltin (TPT) in Cyprinus carpio (C. carpio). The fish (average weight of 56.9±0.4 g) were divided into 4 groups with four replicates: the control, TPT, SFN+TPT and SFN groups. Twenty fish were selected from each tank and cultured for 8 weeks. Then, serum and liver samples were collected for physiological, biochemical and metabolomic analyses. In the present study, TPT downregulated the expression of the lysozyme gene, upregulated HSP70 and Hsp90 gene expression, and decreased the activities of serum antioxidant enzymes (SOD, CAT, and GPX). However, dietary SFN alleviated oxidative stress, and prevented changes in immune genes. Metabolomic analysis revealed that TPT exposure changed key metabolites in the main phenylalanine, fatty acid and glycerophosphatide metabolic pathways, which are related to inflammation, oxidative stress and immunity and might also lead to an imbalance of liver energy and lipid metabolism. Dietary SFN promoted amino acid metabolism and increased metabolites related to immunity, anti-inflammation, antioxidation, and protein synthesis in liver of C. carpio. In summary, dietary SFN supplementation reversed TPT-induced decreases in immunity and oxidative stress and regulated amino acid metabolism, lipid metabolism, inflammation and immunity-related metabolic pathways.

Exploring the mechanism of intestinal injury induced by Bisphenol S in freshwater crayfish (Procambarus clarkii): Molecular and biochemical approaches.

Bisphenol S (BPS) is extensively utilized in various industries such as plastic manufacturing, food packaging, and electronics. The release of BPS into aquatic environments has been observed to have negative impacts on aquatic ecosystems. Research has shown that exposure to BPS can have adverse effects on the health of aquatic animals. This study aimed to explore the mechanism of oxidative stress and endoplasmic reticulum stress induced in freshwater crayfish (Procambarus clarkii) by exposure to BPS (0 µg/L, 1 µg/L, 10 µg/L, and 100 µg/L) for 14 days. The results showed that BPS exposure resulted in elevated levels of reactive oxygen species (ROS) and malondialdehyde (MDA) and severe intestinal histological damage. In addition, oxidative stress can occur in the body by inhibiting the activity of antioxidant enzymes and the expression of related genes. BPS exposure induced a significant increase in the relative mRNA expression levels of inflammatory cytokines (NF-κB and TNF-α) and key unfolded protein response (UPR) related genes (Bip, Ire1, and Xbp1). At the same time, BPS exposure also induced up-regulation of apoptosis genes (Cytc and Casp3), suggesting that UPR and Nrf2-Keap1 signaling pathways may play a protective role in the process of apoptosis and oxidative stress. In conclusion, Our findings present the initial evidence that exposure to environmentally relevant levels of BPS can lead to intestinal injury through various pathways, highlighting concerns about the potential harm at a population level from BPS and other bisphenol analogs.

Bisphenol S exposed changes in intestinal microflora and metabolomics of freshwater crayfish, Procambarus clarkii.

Bisphenol S (BPS), a typical endocrine-disrupting chemical (EDC), can cause hepatopancreas damage and intestinal flora disturbance. Comprehensive studies on the mechanisms of acute toxicity in crustaceans are lacking. In this study, 16S rRNA and liquid chromatography were used to investigate intestinal microbiota and metabolites of freshwater crayfish (Procambarus clarkii). In this study, freshwater crayfish were exposed to BPS (10 µg/L and 100 µg/L). The results showed a significant decrease in catalase (CAT) and superoxide dismutase (SOD) activities after exposure to BPS, which inhibited the Nrf2-Keap1 signaling pathway and induced oxidative stress toxicity in freshwater crayfish. In addition, BPS exposure induced the structural changes of intestinal microbial in the freshwater crayfish, showing different patterns of effects. The number of potentially pathogenic bacteria increased, such as Citrobacter, Hafnia-Obesumbacterium, and RsaHf231. A total of 128 different metabolites were analyzed by LC-MS/MS. The inositol and leukotriene (LT) contents in the hepatopancreas of freshwater crayfish were significantly decreased after 10 µg/L BPS exposure, which in turn led to the accumulation of lipids causing hepatopancreas damage. In conclusion, when the concentration of BPS in the water environment exceeded 10 µg/L, the freshwater crayfish intestinal microbiota was dysbiosis and the hepatopancreas metabolism was disturbed.

The effects of bisphenol S exposure on the growth, physiological and biochemical indices, and ecdysteroid receptor gene expression in red swamp crayfish, Procambarus clarkii.

The experiment was conducted to investigate the effects of Bisphenol S (BPS) on growth, physiological and biochemical indices, and the expression of ecdysteroid receptor (ECR) of the red swamp crayfish (Procambarus clarkii). The gene encoding ECR was isolated from red swamp crayfish by homologous cloning and rapid amplification of cDNA ends (RACE). The ECR transcripts were 1757 bp long and encoded proteins of 576 amino acids. The quantitative real-time PCR (qRT-PCR) analysis showed that the ECR gene was expressed in various tissues under normal conditions, and the highest level was observed in the ovary and the lowest level was observed in the muscle (P < 0.05). Then, the experiment was designed with four different BPS concentrations (0, 1, 10, and 100 µg/L), BPS exposure for 14 days, three parallel groups, and a total of 240 red swamp crayfish. At 100 µg/L BPS, the survival rate, weight gain rate, and relative length rate were decreased significantly (P < 0.05). Malonaldehyde (MDA) content reached the highest level at 100 µg/L BPS. When BPS concentration was higher than 10 µg/L, the activities of superoxide dismutase (SOD) and catalase (CAT) were significantly lower than those of the control group (P < 0.05). The expression levels of the ECR gene in ovary, intestinal, gill, and hepatopancreas tissues were significantly increased after BPS exposure (P < 0.05). The ECR gene expression in ovaries and Y-organs was significantly higher than other groups in 10 µg/L BPS (P < 0.05). The expressions of the tumor necrosis factor -α (TNF-α) and interleukin-6 (IL-6) genes in the hepatopancreas gradually increased, and the highest expression was observed exposed in 100 µg/L BPS (P < 0.05). This research will provide novel insights into the health risk assessment of BPS in aquatic organisms.

Protective effects of sulforaphane on inflammation, oxidative stress and intestinal dysbacteriosis induced by triphenyltin in Cyprinus carpio haematopterus.

The purpose of this experiment was to study the mitigation effect of sulforaphane (SFN) on fish toxicological damage caused by triphenyltin (TPT) pollution. A total of 320 healthy fish (56.9 ± 0.4g) were randomly placed into four groups, each with four duplicates. The control group was fed the basal diet, the TPT group was exposed to 10 ng/L TPT on the basis of the control group, the SFN group was fed a diet supplemented with 10 mg/kg SFN, the SFN + TPT group was exposed to 10 ng/L TPT on the basis of the SFN group. Each tank had 20 fish and the breeding lasted for 8 weeks. The present study found that the antioxidant enzyme activity in the TPT group was significantly lower than that of the control group (P < 0.05). In addition, compared with the control group, the mRNA expression of pro-inflammatory factors (IL-6, TNF-α) were significantly induced, and the anti-inflammatory factor genes (IL-10, TGF) were significantly inhibited (P < 0.05) in TPT group. SFN relieved the changes of inflammatory factors caused by TPT, ameliorated oxidative stress, improved antioxidant enzyme (include SOD, CAT, GSH, GPx) activities (P < 0.05). 16s RNA analysis indicated that exposure to TPT caused changes in intestinal microflora. The results of the study showed that after exposure to TPT, some beneficial genera of bacteria in the gut of Rhizobiaceae, Bdellovibrio and Candidatus Alysiosphaera were decreased. The bacteria associated with intestinal inflammation including Propionibacterium, Rubrobacter, Anaerorhabdus_furcosa_group, Rikenellaceae and Eubacterium_brachy were upregulated. However, the SFN treatment group significantly down-regulated the above five inflammation-related bacteria. The above results indicated that TPT caused oxidative stress and inflammation in fish intestines, changed the intestinal microflora, and dietary SFN could improve antioxidant status, regulate inflammation and intestinal health. Therefore, SFN is a promising diet additive for improving fish damage caused by TPT contamination.

Effects of ammonia exposure on anxiety behavior, oxidative stress and inflammation in guppy (Poecilia reticulate).

Ammonia is one of the most important aquatic environmental factors, which is of great concern. In order to evaluate the effect of ammonia on guppy (Poecilia reticulate), fish were exposed to increased concentrations (0, 12.50, 25.00, 41.67, 62.50 mg/L) of ammonia for 48 h. After exposure, we measured the anxiety behavior, antioxidant enzymes and pro-inflammation genes (TNF-α, IL-1ß and IL-6) of guppy. The results showed that ammonia stress induced fish anxiety, which was manifested by the increased latency to enter the upper half and decreased time spent in upper half compared with control fish. The guppy showed oxidative stress after 48 h of ammonia stress as evidenced by decreases in the activities of antioxidant enzymes and an increase in lipid hydroperoxide content. With prolonged ammonia stress, the expressions of HSP70, HSP90, TNF-α, IL-1ß and IL-6 mRNA at first had an increasing trend, and then decreased, all of which were significantly higher than the control levels at 12 h and 24 h after ammonia stress (P < 0.05). Ammonia significantly upregulated these genes mRNA levels after 48 h exposure, suggesting that heat shock proteins and innate immune system may try to protect cells from oxidative stress induced by ammonia stress. Our study showed that higher ammonia exposure induced oxidative stress in exposed fish, since inhibition of antioxidant enzymes activity and increases in lipid peroxidation, and inflammation occurred. Furthermore, the results will be helpful to understand the mechanism of ammonia toxicity in guppys.

Paecilomyces variotii: A Fungus Capable of Removing Ammonia Nitrogen and Inhibiting Ammonia Emission from Manure.

Ammonia (NH3) emissions from animal manure are a significant environmental and public concern. Despite the numerous studies regarding NH3 emissions from manure, few of them have considered microbial nitrification approaches, especially fungal nitrification. In this study, a filamentous fungus was isolated from chicken manure and was used for nitrification. The species was Paecilomyces variotii by morphological characteristics and 18S rDNA gene sequencing. It played the biggest role in the removal of ammonium at pH 4.0-7.0, C/N ratio of 10-40, temperature of 25-37°C, shaking speed of 150 rpm, and with glucose as the available carbon source. Further analysis revealed that all ammonium was removed when the initial ammonium concentration was less than 100 mg/L; 40% ammonium was removed when the initial ammonium concentration was 1100 mg/L. The results showed that the concentration of ammonia from chicken manure with strain Paecilomyces variotii was significantly lower than that in the control group. We concluded that Paecilomyces variotii has good potential for future applications in in situ ammonium removal as well as ammonia emissions control from poultry manure.