- Fluoride induced histological changes in the liver tissue.
- Fluoride induced significant damage to hepatocyte in mice.
- Fluoride caused notable mitochondrial morphological structure change.
- Drp1/Mff signaling pathway was involved in fluoride-induced mitochondria division.
- Fluoride induced apoptosis in hepatocyte.
Fluoride, a toxic substance, is widely distributed in the environment and causes serious damage to the body. This study was performed to investigate the effects of fluoride on mitochondrial fission in mouse hepatocytes. A total of 48 mice were equally divided into four groups and admisnistered with NaF in drinking water at fluorine ion concentrations of 0, 25, 50 and 100 mg/L for 70 days. The pathomorphology and ultrastructurre of hepatocytes were then observed. The mitochondrial lesion parameters (number, length, width and vacuolization area) are evaluated. The expression of Drp1, Mff, Fis1, MiD49, MiD51 and Dyn2, which are associated with mitochondrial fission, was determined by quantitative real-time PCR and Western blot analysis. Apoptosis was detected by using TUNEL assay. Results showed that fluoride causes notable changes in the pathological morphology of liver tissues and severely damages the ultrastructure of hepatocytes. Damage manifested as nuclear condensation, nuclear membrane breakdown, mitochondrial vacuolation, increased fragmentation, and mitochondrial fission. Moreover, mRNA and protein expression levels were significantly upregulated in the Drp1/Mff signaling pathway. The mRNA expression levels of Cyt c, caspase 9 and 3 markedly increased in the fluoride treated groups in a dose-dependent manner. The percentage of TUNEL-positive nuclei in the liver remarkably increased after fluoride treatment. Overall, the results indicate that excessive fluoride exposure can increase mitochondrial fission via the Drp1/Mff signaling pathway, severely damage the mitochondrial structure, and lead to apoptosis of hepatocytes.
*Original abstract online at https://www.sciencedirect.com/science/article/pii/S0048969720317058?via%3Dihub
Effect of the extract from nettle (urtica dioica L.) fruit cluster on the synthesis of pro-inflammatory agents in hepatocytes treated with fluoride
Nettle, Urtica dioica L., is frequently used by humans for medicinal purposes and has antioxidant, anti-inflammatory, and hepatoprotective properties. As no data were available on the effect of nettle extract on the synthesis of pro-inflammatory agents in hepatocytes treated with fluoride, we decided to investigate this. Aqueous and ethanol extracts
The morphological changes and molecular biomarker responses in the liver of fluoride-exposed Bufo gargarizans larvae
Highlights Fluoride triggered marked histological changes in the liver of Bufo gargarizans [the Asiatic toad or Chusan Island toad] Fluoride caused disruption of lipid metabolism. Fluoride resulted in impairing of antioxidant capacity. Fluoride induced alterations of mRNA expression of genes involved in apoptosis. The goal of the current study was to
Proposed mechanism for understanding the dose- and time-dependency of the effects of fluoride in the liver.
Fluoride (F) can induce changes in the expression of several liver proteins.It is suggested that these changes are dose- and time-dependent. The objective of this study was to analyze the effect of different F concentrations and exposure times to this ion on the pattern of protein expression in the liver
Apoptotic and Oxidative Mechanisms in Liver and Kidney Tissues of Sheep with Fluorosis.
This study was planned to determine the molecular basis and causes of damage to the kidney and the liver, which are the most affected tissues in sheep exposed to chronic fluoride. For this purpose, liver and kidney tissues were obtained from sheep with signs of fluorosis in the age range
Sodium Fluoride (NaF) Induces Inflammatory Responses Via Activating MAPKs/NF-kB Signaling Pathway and Reducing Anti-inflammatory Cytokine Expression in the Mouse Liver.
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