- Sodium fluoride exhibited toxic effect on isolated rat liver mitochondria.
- N-Acetylcysteine protected against the fluoride toxicity on mitochondria.
- Interfering of fluoride with the mitochondrial functionality can be the result of oxidative stress and subsequent collapse of mitochondrial membrane potential (??m).
Fluoride is abundant in the environment and exists mostly in combination with other elements as fluoride compounds. Several studies showed that exposing to irregular level of fluoride could impair the normal function of mitochondria that have major contribution for producing of reactive oxygen species (ROS). However, information about the exact mechanism behind the fluoride-induced mitochondrial damage has not been fully understood. In the present study, isolated rat liver mitochondria were exposed to different concentrations of sodium fluoride (NaF) for 30?minutes and their functionality was assessed at the presence of different concentrations of N-acetylcysteine (NAC) and IC50 concentration of NaF. Mitochondrial dehydrogenase activity, glutathione (GSH) content, lipid peroxidation, ROS production and mitochondrial membrane potential (MMP) assay in the presence of these two substances were evaluated. Our findings demonstrated that, NaF reduced the GSH content of mitochondria, increased ROS and lipid peroxidation which led to a decrease in the dehydrogenase activity (complex II) of mitochondria. NAC considerably inhibited those noxious effects of NaF on mitochondria and prevented NaF toxicity on mitochondria isolated from rat liver.
*Original abstract online at https://www.sciencedirect.com/science/article/abs/pii/S0022113920303341
Co-exposure to non-toxic levels of cadmium and fluoride induces hepatotoxicity in rats via triggering mitochondrial oxidative damage, apoptosis, and NF-kB pathways.
Fluoride (F) and cadmium (Cd) are two common water pollutants. There is low information about their co-exposure in low doses. So, in this study, we evaluated the combination effects of non-toxic doses of F and Cd and the possible mechanism of their combined interaction. Male rats were exposed to non-toxic
Genotoxic effect and rat hepatocyte death occurred after oxidative stress induction and antioxidant gene downregulation caused by long term fluoride exposure
Studies focusing on possible genotoxic effects of excess fluoride are contradictory and inconclusive. Currently, studies have reported a probable link to oxidative stress, DNA damage and apoptosis induced by fluoride in rat hepatocytes. We developed an in vivostudy administering three doses of fluoride by gavage given to rats for 60 day.
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
Changes in adrenal function as a possible mechanism for elevation of serum glucose by a single large dose of fluoride.
Serum glucose was elevated immediately after ip administration of a single large dose of fluoride (NaF 35 mg/kg) to rats. Moreover, elevation of serum glucose following ip administration of 35 mg/kg of fluoride to rats was suppressed by adrenalectomy, dibenamine, or propranolol, but not by thyroid-parathyroidectomy. The elevation of serum
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
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