- 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
Exocyclic DNA adducts in sheep with skeletal fluorosis resident in the proximity to the Portoscuso-Portovesme industrial estate on Sardinia Island, Italy
The mechanisms by which fluoride produces its toxic effects are still not clear. Therefore, we conducted a cross-sectional study to evaluate the fluoride-induced toxicity on randomly selected sheep with skeletal fluorosis resident near the large non-ferrous metallurgy Portoscuso-Portovesme industrial estate and the Carbonia and Gonnessa towns (control district) in respect
Fluoride intoxication and possible changes in mitochondrial membrane microviscosity and organ histology in rats
Fluoride exposure to rats can alter system physiology and biochemistry and results in abnormal organ function. Mitochondria, the power house of the cell can be act as a marker to identify fluoride mediated oxidative damage through changes of mitochondrial micro viscosity. Male albino rats were fed with 5 ppm, 10
Correlations between fluoride concentration and free radical parameters in soft tissues of rats.
In previous studies we investigated the impact of subchronic exposure of rats to sodium fluoride administered in their drinking water as it affected selected biochemical parameters in their soft tissues and organs. The activity of glutathione peroxidase and the concentrations of fluoride, reduced glutathione (GSH), substances reacting with thiobarbituric acid (TBARS), and carbonyl groups were determined in kidney,
[The influence of methionine and vitamin E on oxidative stress in rats’ liver exposed to sodium fluoride]
BACKGROUND: Fluorine influences many processes occurring in the organism. Controversies over the evaluation of the biological effects of this substance are due to a small difference between tolerable and toxic fluorine doses. One of the main mechanisms of the fluorine toxic action is its ability to induce oxidative stress via
A possible mechanism for combined arsenic and fluoride induced cellular and DNA damage in mice
Arsenic and fluoride are major contaminants of drinking water. Mechanisms of toxicity following individual exposure to arsenic or fluoride are well known. However, it is not explicit how combined exposure to arsenic and fluoride leads to cellular and/or DNA damage. The present study was planned to assess (i) oxidative stress
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