Effect of Fluoride on Cytotoxicity Involved in Mitochondrial Dysfunction: A Review of Mechanism

Abstract

Fluoride is commonly found in the soil and water environment and may act as chronic poison. A large amount of fluoride deposition causes serious harm to the ecological environment and human health. Mitochondrial dysfunction is a shared feature of fluorosis, and numerous studies reported this phenomenon in different model systems. More and more evidence shows that the functions of mitochondria play an extremely influential role in the organs and tissues after fluorosis. Fluoride invades into cells and mainly damages mitochondria, resulting in decreased activity of mitochondrial related enzymes, weakening of protein expression, damage of respiratory chain, excessive fission, disturbance of fusion, disorder of calcium regulation, resulting in the decrease of intracellular ATP and the accumulation of Reactive oxygen species. At the same time, the decrease of mitochondrial membrane potential leads to the release of Cyt c, causing a series of caspase cascade reactions and resulting in apoptosis. This article mainly reviews the mechanism of cytotoxicity related to mitochondrial dysfunction after fluorosis. A series of mitochondrial dysfunction caused by fluorosis, such as mitochondrial dynamics, mitochondrial Reactive oxygen species, mitochondrial fission, mitochondrial respiratory chain, mitochondrial autophagy apoptosis, mitochondrial fusion disturbance, mitochondrial calcium regulation are emphasized, and the mechanism of the effect of fluoride on cytotoxicity related to mitochondrial dysfunction are further explored.

Biocompatible and Oxidation‐Resistant Ti3C2Tx MXene with Halogen‐Free Surface Terminations

“…Fions in concentrations exceeding 100 ppm can be toxic for promoting the generation of reactive oxygen species, and possibly explain the cytotoxic results in MILD-Ti 3 C 2 T x . [84,85] In addition, cell staining and flow cytometry analysis were also carried out using live/dead and apoptosis assay kit in living cells after treating with 72-h-aged NaOH-Ti 3 C 2 T x and MILD-Ti 3 C 2 T x which the cell viability assays started to deviate significantly. The micrographs showed that most cells were viable in the NaOH-Ti 3 C 2 T x MXene treated group as the dead cells with red fluorescence were hardly observed (Figure 5e).…”

“…F – ions in concentrations exceeding 100 ppm can be toxic for promoting the generation of reactive oxygen species, and possibly explain the cytotoxic results in MILD‐Ti 3 C 2 T x . [ 84,85 ]…”

Modified Linggui Zhugan Decoction protects against ventricular remodeling through ameliorating mitochondrial damage in post-myocardial infarction rats

“…Specifically, rupture of the outer mitochondrial membrane leads to Cyt c release from the intermembrane space and subsequent inner mitochondrial membrane depolarization ( 56 ). At the same time, mitochondrial membrane potential(MMP) decrease, in turn, leads to Cyt c release ( 57 ). In the cytoplasm, apoptosomes formed with Cyt c, apoptotic protease-activating factor 1 (Apaf-1), and caspase-9 trigger caspase-3 activation, ultimately leading to apoptosis ( 10 , 58 ).…”

Sodium fluoride induces skeletal muscle atrophy via changes in mitochondrial and sarcomeric proteomes

“…Mitochondrial complexes I, II, and III, play an important role in regulating mitochondrial function and ATP production and are the main checkpoints for electron entry into the mitochondrial electron transport chain [ 56 , 57 ], where the entry and exit of the ions inside and outside the membrane take place. NaF treatment at a low or high concentration for a short period increases the mitochondrial activity of the complex-I, as shown in our study ( Fig 4 , Table 1 ).…”