Sodium fluoride induced skeletal muscle changes: Degradation of proteins and signaling mechanism

Shenoy, Prashanth; Sen, Utsav; Kapoor, Saketh; Ranade, Anu Vinod; Chowdhury, Chitta Ranjan; Bose, Bipasha

doi:10.1016/j.envpol.2018.10.034

Cited by 23 publications

(8 citation statements)

References 61 publications

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“…Further, as the concentration of NaF increases (5ppm), the accumulation of ubiquitinated proteins increases, indicating that proteasome-related proteolysis was enhanced. In our previous study [5,50] we saw an increase in the expression of muscle transcription factor MyoD at the same concentration (1.5ppm; low concentration and early time point) in C2C12 myoblast and C57BL6 mouse muscle was exposed to NaF. This suggests the critical role played by UPS in muscle regeneration.…”

Section: Plos Onementioning

confidence: 80%

“…Skeletal fluorosis is characterized by the thickening of the periosteum, calcification of muscle, tendons, ligaments, and multiple hypertrophic bony projections near the ligament and atrophic muscle attachments to bone [4]. Along with bone, muscles get affected by fluorosis, and muscles change (hypertrophy and atrophy) depending upon the fluoride dose and exposure period [5][6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2022

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Sodium Fluoride (NaF) can change the expression of skeletal muscle proteins. Since skeletal muscle is rich in mitochondrial and contractile (sarcomeric) proteins, these proteins are sensitive to the effects of NaF, and the changes are dose-and time-dependent. In the current study, we have analysed the effect of high concentrations of NaF (80ppm) on mouse skeletal muscle at two different time points, i.e., 15 days and 60 days. At the end of the experimental time, the animals were sacrificed, skeletal muscles were isolated, and proteins were extracted and subjected to bioinformatic (Mass Spectrometric) analysis. The results were analysed based on changes in different mitochondrial complexes, contractile (sarcomeric) proteins, 26S proteasome, and ubiquitin-proteasome pathway. The results showed that the mitochondrial proteins of complex I, II, III, IV and V were differentially regulated in the groups treated with 80ppm of NaF for 15 days and 60 days. The network analysis indicated more changes in mitochondrial proteins in the group treated with the higher dose for 15 days rather than 60 days. Furthermore, differential expression of (sarcomeric) proteins, downregulation of 26S proteasome subunits, and differential expression in proteins related to the ubiquitin-proteasome pathway lead to muscle atrophy. The differential expression might be due to the adaptative mechanism to counteract the deleterious effects of NaF on energy metabolism. Data are available via ProteomeXchange with identifier PXD035014.

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Section: Plos Onementioning

confidence: 80%

Section: Introductionmentioning

confidence: 99%

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

et al. 2022

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“…Shenoy et al, [42] assessed the effect of NaF administration at different concentrations on myoblast proliferation. In contrast our study where NaF was administered at a dose of 25mg/kg, the author concluded that at a low concentration of 1.5 ppm (1 ppm being equivalent to 1 mg/kg), NaF administration resulted in myoblast proliferation and myotubular hypertrophy via an IGF-1/AKT pathway activation, whereas at a higher concentration of 5 ppm, NaF caused myotubular atrophy via an ubiquitin-proteosome pathway.…”

Section: Discussionmentioning

confidence: 99%

Keap1/Nrf2 pathway in sodium fluoride-induced cardiac toxicity and the prophylactic role of vitamin C versus platelet-rich plasma

et al. 2022

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The present study was conducted to investigate the role of vitamin C versus platelet-rich plasma against sodium fluoride (NaF)-induced cardiotoxicity and cell death in rats' myocardium.Previous studies suggest that NaF decreased cellular viability and intracellular antioxidant power. The present study revealed that NaF administration caused histological alterations in the cardiac muscle and increased the accumulation of intracellular reactive oxygen species, the expression of iNOS and PCNA as well as collagen deposition in cardiac tissue. As supported by colorimetric analysis, an elevation in MDA level and a decrease in both SOD and TrX levels were seen, whereas molecular analysis revealed a decrease in Keap1 and an increase in Nrf2 and HO-1 gene expression. Pretreatment with vitamin C and PRP prior to NaF administration significantly improved the altered parameters and enhanced the cellular antioxidant capability of myocardium resulting in protection of cardiac muscle from NaF-induced cytotoxicity and apoptotic cell death. The cyto-protective activity of PRP was found to be comparable to that of the known antioxidant, vitamin C.

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“…The effects of fluoride are biphasic. Exposing human dental pulp cells to a low concentration of NaF (25 µM-50 µM) stimulated proliferation and differentiation, while a concentration of NaF at 50 µM to 100 µM stimulated proliferation, differentiation, and collagen synthesis in human osteoblastic osteosarcoma cells [7]. Myoblasts exposed to low concentrations of NaF promoted proliferation, which could be regarded as a muscle enhancing factor, and high concentrations elevated the expression of muscle atrophyrelated genes, myostatin and atrogin-1, reactive oxygen species (ROS), and inflammatory factors that accelerate skeletal muscle atrophy [8].…”

Section: Introductionmentioning

confidence: 99%

Biphasic Functions of Sodium Fluoride (NaF) in Soft and in Hard Periodontal Tissues

Wang

Tewari

Sato

et al. 2022

IJMS

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Sodium fluoride (NaF) is widely used in clinical dentistry. However, the administration of high or low concentrations of NaF has various functions in different tissues. Understanding the mechanisms of the different effects of NaF will help to optimize its use in clinical applications. Studies of NaF and epithelial cells, osteoblasts, osteoclasts, and periodontal cells have suggested the significant roles of fluoride treatment. In this review, we summarize recent studies on the biphasic functions of NaF that are related to both soft and hard periodontal tissues, multiple diseases, and clinical dentistry.

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Sodium fluoride induced skeletal muscle changes: Degradation of proteins and signaling mechanism

Cited by 23 publications

References 61 publications

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

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

Keap1/Nrf2 pathway in sodium fluoride-induced cardiac toxicity and the prophylactic role of vitamin C versus platelet-rich plasma

Biphasic Functions of Sodium Fluoride (NaF) in Soft and in Hard Periodontal Tissues

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