- 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
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
Lipid peroxidation in fluorosis and the protective role of dietary factors
The influence of chronic Fl intoxication on lipid peroxidation and the state of the antioxidant system was studied in rats on different diets. Chronic Fl intoxication inhibited antioxidant activity and caused an increase in the rate of peroxidation and the level of lipoperoxides in liver, brain and serum. Diets with
Evaluation of caspase-dependent apoptosis during fluoride-induced liver lesion in pigs
Sixteen barrows (Duroc x Landrace x Yorkshire) were randomly divided into two groups, each consisting eight pigs. The groups received the same basal diet supplemented with 0 and 400 mg/kg fluoride, respectively. Histological examinations, including in situ terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), Haematoxylin and Eosin staining (HE)
Sesamin attenuates histological alterations, oxidative stress and expressions of immune-related genes in liver of zebrafish (Danio rerio) exposed to fluoride.
Highlights Sesamin alleviated histological damage and oxidative stress in liver. Sesamin remarkably inhibited the inflammatory reaction in fluoride-exposed liver. Sesamin reversed activities of immune-related enzymes in fluoride-exposed liver. Sesamin reversed expressions of immune-related mRNAs liver exposed to fluoride. Sesamin could protect liver against fluoride-induced damage. Sesamin is the main lignan in
In vivo protective effects of quercetin against sodium fluoride-induced oxidative stress in the hepatic tissue
The protective effects of quercetin against sodium fluoride induced oxidative stress were examined in rat’s liver. Rats were divided into five groups. The first group served as normal group that was treated with standard diet. The second group was intoxicated with sodium fluoride (600 ppm) through drinking water for 1 week. The
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