Abstract
We have demonstrated that degranulation from normal human neutrophils in whole blood was stimulated by low concentrations of lithium salts and was produced by noncytolytic means. Significant amounts of beta-glucuronidase could be released from the primary granules, in addition to vitamin B12- binding protein from the secondary granules, by 10 mM lithium. Release was almost totally inhibited by 1 mM fluoride, under the same conditions. There was no release of lactate dehydrogenase and no loss of viability of cells incubated in either lithium or fluoride at the concentrations used. Lithium was also observed to have no effect on reactive oxygen production by phagocytic stimulation of isolated neutrophils. In addition, lithium and fluoride were shown to manipulate the intracellular levels of cAMP. The results demonstrated a direct effect of lithium on release of inflammatory mediators from neutrophils in vitro. The methods used also provide a simple and effective test to study an important function of neutrophil activity and can be used to evaluate degranulation in a number of clinical conditions.
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Activation of phospholipase A(2) by low levels of fluoride in THP1 macrophages via altered Ca(2+) and cAMP concentration
Phospholipases (PLA's) participate in the regulation of physiological and pathological processes in the cell, including the release of pro-inflammatory mediators and stimulation of inflammatory processes. It is also well known that fluoride can increase the inflammatory reactions. Therefore we decided to examine the effect of fluorides in concentrations determined in
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Stimulation of cAMP accumulation and superoxide production in human neutrophils and monocytes
The effect of sodium fluoride (NaF) on superoxide generation and cyclic adenosine monophosphate (cAMP) levels in human neutrophils and monocytes was investigated. NaF (greater than 10 mM) stimulated superoxide (O2-) production in both cell types in a time dependent manner. NaF (0.5 to 20 mM) increased cAMP levels by 1.5-
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Sodium fluoride evoked histamine release from mast cells. A study of cyclic AMP levels and effects of catecholamines
Calcium triggers the secretion of histamine from mast cells after previous exposure to sodium fluoride. The secretory process can be divided into a fluoride-activation step and a calcium-induced secretory step. It was observed that the fluoride-activation step is accompanied by an elevation of cAMP levels within the cells. The attained
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Effect of fluorine containing compounds on the activity of glycolytic enzymes in rat hepatocytes.
Inhibition of three glycolytic enzymes by NaF and Na2PO3F? in isolated rat hepatocytes has been demonstrated. The data indicate that incubation of hepatocytes with NaF or MFP and subsequent removal of NaF and MFP results in a significant inhibition of enolase (E.C. 4.2.1.11), phosphoglucomutase (E.C. 2.7.5.1.), and pyruvate kinase (E.C.
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Fluoride-elicited developmental testicular toxicity in rats: roles of endoplasmic reticulum stress and inflammatory response
Long-term excessive fluoride intake is known to be toxic and can damage a variety of organs and tissues in the human body. However, the molecular mechanisms underlying fluoride-induced male reproductive toxicity are not well understood. In this study, we used a rat model to simulate the situations of human exposure
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Is the Ingestion of Fluoride an Immunosuppressive Practice?
This paper records several observations which suggest that habitual ingestion of small doses of fluoride, even as small as the 1 mg/L contained in fluoridated water, may decrease the function of the immune system.
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Does Fluoride Ingestion Affect Developing Immune System Cells?
Considerations, supported by some published experimental evidence, suggest that fluoride released during the resorption of high-fluoride bone may produce detrimental effects not only on bone cells but on developing cells of the immune system.
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Fluoride & the Immune System - Summation from the US National Research Council (2006)
“There is no question that fluoride can affect the cells involved in providing immune responses. The question is what proportion, if any, of the population consuming drinking water containing fluoride at 4.0 mg/L on a regular basis will have their immune systems compromised? Not a single epidemiologic study has investigated whether fluoride in the drinking water at 4 mg/L is associated with changes in immune function. Nor has any study examined whether a person with an immunodeficiency disease can tolerate fluoride ingestion from drinking water.”
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