Comparative proteomic analysis of fluoride treated rat bone provides new insights into the molecular mechanisms of fluoride toxicity

Yan, Wei; Zeng, Beibei; Zhang, Hua; Chen, Cheng; Wu, Yanli; Wang, Nanlan; Wu, Yanqiu; Zhao, Donghong; Zhao, Yuxi; Iqbal, Javed; Shen, Liming

doi:10.1016/j.toxlet.2018.04.006

Cited by 28 publications

(10 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the other hand, ATP synthesis was decreased after 10 days of F exposure on U87 glial cells both at 0.019 and 0.22μg/mL. Several studies have already shown that F can act as a mitochondrial toxin in both animal and cell culture models, but the full understanding of how this ion damages the mitochondrial remains unknown [ 40 , 43 – 47 ]. Mitochondrial changes lead to impairment on normal respiratory chain function mediated by Na+/K+-ATPase inhibition and decreased ATP production [ 48 – 51 ].…”

Section: Discussionmentioning

confidence: 99%

Human cultured IMR-32 neuronal-like and U87 glial-like cells have different patterns of toxicity under fluoride exposure

et al. 2021

View full text Add to dashboard Cite

Background Fluoride (F) is a naturally exists in nature but several studies have indicated it as an environmental toxicant to all leaving beings. Human F exposure has increased over the years since this ion has been used by industry on foods, beverages, toothpastes and on water supply. Although F is safe at optimal concentrations in water supply, human exposure to high levels could trigger neurofunctional deficits. Materials and methods In this study, human glial-like (U87) and neuronal-like (IMR-32) cells lineages were used to access F toxicity and CNS cell sensibility on both cell facing the same protocol. Cells were exposed to F over 3, 5 and 10 days on two different F concentrations. Fluoride exposed cells were evaluated by standard toxicity assays to cell viability, apoptosis, necrosis and general cell metabolism. Oxidative stress parameters were evaluated by ATP and ROS levels, lipid peroxidation, GSH/GSSG ratio and comet assay. Results No changes were observed in IMR-32 at any given time while after 10 days of exposure to 0.22μg/mL, U87 glial-like cells showed signs of toxicity such as decreased cell viability by necrosis while general cell metabolism was increased. Oxidative stress parameters were next evaluated only on U87 glial-like cells after 10 days of exposure. F induced a decrease on ATP levels while no changes were observed on reactive oxygen species and lipid peroxidation. GSH/GSSG ratio was decreased followed by DNA damage both on 0.22μg/mL F. Conclusions Our results suggest an important differential behavior of the distinct types of cells exposed to the different fluoride concentrations, pointing that the U87 glial-like cells as more susceptible to damage triggered by this ion.

show abstract

Section: Discussionmentioning

confidence: 99%

Human cultured IMR-32 neuronal-like and U87 glial-like cells have different patterns of toxicity under fluoride exposure

et al. 2021

View full text Add to dashboard Cite

show abstract

“…In addition, the increase in intracellular reactive oxygen species (ROS), as a signal of oxidative stress, can also activate the apoptosis signal pathway. Once the apoptosis stimulation signal occurs, excessive ROS production contributes to macromolecular oxidation, causing free radicals to attack membrane phospholipids, resulting in membrane damage ( 129 ) by inducing lipid peroxidation, mitochondrial membrane depolarization and apoptosis. Sodium fluoride can increase the amount of cAMP and promote apoptosis.…”

Section: Potential Molecular Mechanism Of Mitochondrial Dysfunction I...mentioning

confidence: 99%

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

Wei

Ali

et al. 2022

Front. Vet. Sci.

View full text Add to dashboard Cite

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.

show abstract

“…Bioinformatics analysis was performed by using OMICSBEAN online tools (http://www.omicsbean.cn/) and String (Search Tool for the Retrieval of Interacting Genes/Proteins, version 9.1, http:// string-db.org/) database. DEPs were analyzed by GO (gene ontology) annotation, KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways, and protein-protein interaction (PPI) networks (Iqbal et al, 2018;Wei et al, 2018). Functional interaction network analysis was conducted using the ClueGO Cytoscape plugin (Bindea et al, 2009).…”

Section: Bioinformatics Analysismentioning

confidence: 99%

Protective Effect of Dictyophora Polysaccharides on Sodium Arsenite-Induced Hepatotoxicity: A Proteomics Study

Shen

Huang

et al. 2021

Front. Pharmacol.

Self Cite

View full text Add to dashboard Cite

The purpose of this study is to understand the mechanism of sodium arsenite (NaAsO2)-induced apoptosis of L-02 human hepatic cells, and how Dictyophora polysaccharide (DIP) protects L-02 cells from arsenic-induced apoptosis. The results revealed that DIP pretreatment inhibited NaAsO2 induced L-02 cells apoptosis by increasing anti-apoptotic Bcl-2 expression and decreasing pro-apoptotic Bax expression. Proteomic analysis showed that arsenic treatment disrupted the expression of metabolism and apoptosis associated proteins, including ribosomal proteins (RPs). After pretreatment with DIP, the expression levels of these proteins were reversed or restored. For the first time, it was observed that the significant decrease of cytoplasmic RPs and the increase of mitochondrial RPs were related to human normal cell apoptosis induced by arsenic. This is also the first report that the protective effect of DIP on cells was related to RPs. The results highlight the relationship between RPs and apoptosis, as well as the relationship between RPs and DIP attenuating arsenic-induced apoptosis.

show abstract

Comparative proteomic analysis of fluoride treated rat bone provides new insights into the molecular mechanisms of fluoride toxicity

Cited by 28 publications

References 53 publications

Human cultured IMR-32 neuronal-like and U87 glial-like cells have different patterns of toxicity under fluoride exposure

Human cultured IMR-32 neuronal-like and U87 glial-like cells have different patterns of toxicity under fluoride exposure

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

Protective Effect of Dictyophora Polysaccharides on Sodium Arsenite-Induced Hepatotoxicity: A Proteomics Study

Contact Info

Product

Resources

About