Fluoride Exposure Induces Inhibition of Sodium-and Potassium-Activated Adenosine Triphosphatase (Na+, K+-ATPase) Enzyme Activity: Molecular Mechanisms and Implications for Public Health
Abstract
:1. Introduction
2. The Role of Fluoride in Oral Health and Sources of Fluoride Exposure
Non Fluoridated Region mg/L | Fluoridated Region mg/L | Reference | |
---|---|---|---|
Human milk | 0.004 | 0.009 | [154,161] |
Cow’s Milk | 0.016 | 0.074–0.18 | [156] |
Cow’s milk based powdered | 0.02–0.18 | 0.49–1.40 | [159] |
infant formula reconstituted | |||
with tap water | |||
Non-Fluoridated | Fluoridated | Reference | |
Ionic F levels | Ionic F levels | ||
µM | µM | ||
Fully Breast-fed infants | |||
1–6 months | = 0.22 | [163] | |
Formula fed | |||
1–6 months | = 0.29 | [163] | |
Breast fed with semi solids | |||
6–12 months | = 0.35 | [163] | |
(0.10–0.67) | |||
Aged 1 month | 0.89 | [169] | |
Aged 7 months | 0.53 | [169] | |
Breast and formula fed | |||
Aged 4–6 months | 4.33 | [164] | |
(0.52–8.0) | |||
Aged 7–12 months | 1.56 | [164] | |
with semi solids | (1.03–2.1) | ||
Aged 4–18 months |
3. Na+, K+-ATPase Regulation by Phosphorylation/Dephosphorylation
4. Molecular Mechanisms by which Fluoride Inhibits Na+, K+-ATPase Activity
4.1. The Role of Protein Kinase RNA-like ER Kinase (PERK) in Regulating Na+, K+-ATPase Activity and the Influence of Fluoride on PERK Activity
4.2. The role of Protein Kinase C (PKC) in Regulating Na+, K+-ATPase Activity and the Influence of Fluoride in Regulating PKC Activity
4.3. The Role of Cyclic Adenosine-Monophosphate (cAMP) in Regulating Na+, K+-ATPase Activity and the Influence of Fluoride in Regulating cAMP
4.4. The Influence of Magnesium in Regulating Na+, K+-ATPase Activity and the Influence of Fluoride on Magnesium Homeostasis
4.5. The Influence of Calcineurin, Calmodulin and Manganese in Regulating Na+, K+-ATPase Activity and the Influence of Fluoride on Calcineurin, Calmodulin and Manganese Homeostasis
4.6. The Role of Cyclic Guanosine Monophosphate (cGMP) and Nitric Oxide in Regulating Na+, K+-ATPase Activity and the Contribution of Fluoride to Regulating cGMP and Nitric Oxide
4.7. Cytokine TGF-β1 Inhibits NKA Activity
4.8. The Role of Inorganic Phosphate in Regulating Na+, K+-ATPase Activity
4.9. Dopamine Inhibits Na+-K+-ATPase Activity
4.10. Parathyroid Hormone Inhibits Na(+)-K(+)-ATPase Activity
4.11. Hyperglycaemia Inhibits Na+ K+ ATPase Activity via Activation of PGE2 Production
4.12. Advanced Glycation end Products Inhibit Na+ K+ ATPase
5. Discussion
Additional Perspectives
6. Conclusions
Funding
Conflicts of Interest
Abbreviations
AA | Arachidonic Acid |
ATP | Adenosine-triphosphate |
ALP | Alkaline phosphatase |
cAMP | cyclic adenosine-monophosphate monophosphate |
CaM | Calmodulin |
cGMP | Cyclic guanosine monophosphate |
Cn | Calcineurin |
COPD | Chronic obstructive pulmonary disease |
CT | Calcitonin |
F | Fluoride |
Mn | Magnesium |
NKA: | Na+, K+-ATPase |
NO | Nitric oxide |
PKC | Protein kinase C |
Pi | Inorganic phosphate |
PGE2: | Prostaglandin E2 |
PTH | Parathyroid hormone |
PLA2 | Phospholipase A2 |
RAGE | Receptors for advanced glycation end products |
TGF-β1 | Transforming growth factor β 1 |
TSH | Thyroid-stimulating-hormone, also called Thyrotropin |
α | Alpha |
β | Beta |
U.S.A | United States of America |
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Factor | Effect of F− | Effect on Na+, K+-ATPase Activity |
---|---|---|
ATP | ↓ | ATP is required for NKA homeostasis. Lower bioavailability of ATP leads to inhibition of enzyme activity |
ENO1 | ↓ | Enolase is necessary for glycolysis and ATP production. Inhibition of enolase leads to loss of NKA activity |
PKC | ↑ | PKC phosphorylates the α-1 subunit of NKA leading to inhibition of activity. |
cAMP | ↑ | Inhibits NKA activity by decreasing bioavailability of ATP and enhancing phosphorylation of the α-1 subunit of NKA |
Cn | ↓ | Regulates the dephosphorylation of NKA. Phosphorylation of NKA inhibits enzyme activity. Hence, inhibition or activation of Cn regulates enzymatic activity. Requires Calmodulin and Manganese for structural stability and full activity. |
CaM | ↑ | Inhibits Na+, K+-ATPase activity by enhancing phosphorylation |
Mn2+ | ↓ | Mn2+ is also an activator of Cn and its binding to Cn is required for functional stability and enzyme activity. Loss of Mn2+ inhibits Cn expression and impairs Cn activity leading to enhanced phosphorylation of NKA. Phosphorylation inhibits NKA activity. |
Mg2+ | ↓ | Mg2+ facilitates the binding of ATP to NKA thereby providing the chemical energy required for enzyme activity. |
cGMP | ↑ | Inhibits NKA activity |
NO | ↑ | Inhibits NKA activity |
Pi | ↑ | Inhibits NKA activity directly as well as inhibiting the phosphatase activity of Cn. |
RANKL | ↑ | Inhibits NKA indirectly by increasing osteoclast number, bone resorption and Pi release |
ALP | ↑ | ALP regulates Pi release, thereby indirectly inhibiting NKA activity. ALP activity in turn stimulated by Calcitonin. |
TGF-β1 | ↑ | Inhibits NKA activity. Calcitonin has been found to be a potent stimulator of TGF-β1 protein synthesis as well as TGF-β1 mRNA expression. |
CT | ↑ | Inhibits NKA activity indirectly by upregulating TGF-β1 and ALP activity. |
DA | ↑ | Inhibits NKA activity. PKC and cAMP signalling further contribute to dopaminergic inhibition of NKA. |
TRH | ↑ | Inhibits NKA activity indirectly by inducing DA release. |
PTH | ↑ | Inhibits NKA activity directly. PTH also inhibits NKA activity indirectly through activation of PKC, cAMP, PLA2 and PKA dependent pathways. |
PLA2 | ↑ | Inhibits NKA activity. |
PGE2 | ↑ | Inhibits NKA activity. |
BgL | ↑ | Inhibits NKA activity, via activation of PKC, PLA2 and PGE2. |
AGEs | ↑ | Inhibits NKA activity. |
TSH | ↑ | TSH induces cAMP production and cAMP inhibits NKA activity by reducing ATP bioavailability and enhancing phosphorylation of the alpha-1 subunit of NKA |
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Waugh, D.T. Fluoride Exposure Induces Inhibition of Sodium-and Potassium-Activated Adenosine Triphosphatase (Na+, K+-ATPase) Enzyme Activity: Molecular Mechanisms and Implications for Public Health. Int. J. Environ. Res. Public Health 2019, 16, 1427. https://doi.org/10.3390/ijerph16081427
Waugh DT. Fluoride Exposure Induces Inhibition of Sodium-and Potassium-Activated Adenosine Triphosphatase (Na+, K+-ATPase) Enzyme Activity: Molecular Mechanisms and Implications for Public Health. International Journal of Environmental Research and Public Health. 2019; 16(8):1427. https://doi.org/10.3390/ijerph16081427
Chicago/Turabian StyleWaugh, Declan Timothy. 2019. "Fluoride Exposure Induces Inhibition of Sodium-and Potassium-Activated Adenosine Triphosphatase (Na+, K+-ATPase) Enzyme Activity: Molecular Mechanisms and Implications for Public Health" International Journal of Environmental Research and Public Health 16, no. 8: 1427. https://doi.org/10.3390/ijerph16081427