Fluoride compounds are abundant and widely distributed in the environment at various concentrations, which can seriously injure the human body. In this study, we aim to evaluate the effects of excessive fluoride exposure on the liver, kidney, and heart tissues of healthy female Xenopus laevis by administering NaF (0, 100, and 200 mg/L) in drinking water for 90 days. The expression level of procaspase-8, cleaved-caspase-8, and procaspase-3 proteins were determined by Western blot . Compared with the control group, the group exposed to NaF exhibited expression levels of procaspase-8, cleaved-caspase-8, and procaspase-3 proteins that were considerably upregulated at a concentration of 200 mg/L in the liver and kidney. The cleaved-caspase-8 protein expression in the group exposed to a high concentration of NaF was lower than that in the control group in heart. Histopathological results by hematoxylin and eosin staining showed that excessive NaF exposure caused necrosis of hepatocytes and vacuolization degeneration. Granular degeneration and necrosis in renal tubular epithelial cells were also observed. Moreover, hypertrophy of myocardial cells, atrophy of myocardial fibers and disorder of myocardial fibers were detected. These results demonstrated that NaF-induced apoptosis and the mediated death receptor pathway activation ultimately damaged the liver and kidney tissues. This finding offers a fresh perspective on the effects of F-induced apoptosis in X. laevis.
Shuquan Ding,Shunli Che,Mengting Huang,Yuan Ma,Longteng Shen,Jianbin Feng,Xilei Li
Nanopolystyrene (NP) pollution in aquatic environments has become an increasing concern. Phoxim (PHO), one of the major organophosphorus pesticides, has also been detected in aquatic environments, posing serious health risks to crustaceans. This study aimed to assess the detrimental effects of NP and/or PHO exposure at environmentally relevant concentrations on the intestinal histopathology, intestinal microbiota, and metabolome of adult crabs ( Eriocheir sinensis ) for 21 days. Our study revealed significant histopathological abnormalities in the intestines. In all the exposure groups, there was a discovery of vacuolar degeneration occurring in epithelial cells. Additionally, the peritrophic membrane exhibited thinning after NP or PHO single exposure, while thickening was observed after co-exposure. Exposure to NP and/or PHO disrupted the intestinal microbiota homeostasis, as evidenced by the proliferation of pathogenic bacteria and suppression of beneficial bacteria. Notably, PHO exposure resulted in increased abundance of pathogenic bacteria ( Spiroplasma and Arcobacter ) and decreased abundance of beneficial bacteria ( Bacteroides ). Analysis of the metabolome revealed that exposure to NP and/or PHO led to alterations in the metabolic profile as well as several critical pathways. Among these, the upregulation of arachidonic acid metabolism, ABC transporters, and biosynthesis of amino acids was observed in both NP single exposure and co-exposure, while PHO single exposure downregulated these pathways. Additionally, NP and/or PHO exposure downregulated neuroactive ligand-receptor interaction. Spearman correlation analysis revealed that the significant reduction of some differentially expressed metabolites (DEMs) was potentially regulated by the low-abundance bacterial genera following exposure to NP and/or PHO. And these DEMs have a role in anti-inflammatory or antioxidant properties. Collectively, our results offer novel perspectives on the intestinal toxicity of crustaceans by NP and/or PHO at environmentally relevant concentrations.
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