- 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
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