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.