Anna Strunecka

Fluoride Interactions: From Molecules to Disease

Fluoride has long been known to influence the activity of various enzymes in vitro. Later it has been demonstrated that many effects primarily attributed to fluoride are caused by synergistic action of fluoride plus aluminum. Aluminofluoride complexes have been widely used as analogues of phosphate groups to study phosphoryl transfer reactions and heterotrimeric G proteins involvement. A num- ber of reports on their use have appeared, with far-reaching consequences for our understanding of fundamental biological processes. Fluoride plus aluminum send false messages, which are amplified by processes of signal transduction. Many investigations of the long- term administration of fluoride to laboratory animals have demonstrated that fluoride and aluminofluoride complexes can elicit impair- ment of homeostasis, growth, development, cognition, and behavior. Ameliorative effects of calcium, vitamins C, D, and E have been re- ported. Numerous epidemiological, ecological, and clinical studies have shown the effects of fluoride on humans. Millions of people live in endemic fluorosis areas. A review of fluoride interactions from molecules to disease is necessary for a sound scientific assessment of health risks, which may be linked to the chronic intake of small doses of fluoride and aluminum from environmental and artificial sources.

Aluminofluoride Complexes in the Etiology of Alzheimer’s Disease

The question of aluminum’s relevance to the etiology of Alzheimer’s disease cannot yet be adequately answered. The mechanisms of how aluminum could evoke the hallmarks of AD are not known. Reflecting many studies, which utilize aluminofluoride complexes in laboratory investigations, we suggest that these complexes may act as the initial signal stimulating impairment of homeostasis, degeneration, and death of the cells. Aluminum ions in the presence of fluoride can accelerate the aging and impair the functions of the nervous system. In respect to the etiology of Alzheimer’s disease, the long-term synergistic action of aluminum ions and fluorides may represent a hidden but serious and powerful risk factor for the development of this devastating threat to human civilization.

Differential effect of anaerobiosis on phospholipid metabolism in insect muscle

Abstract An in vivo anaerobic exposure of 80 min duration induces little change in the rate of incorporation of 32 P into flight muscle phospholipids of male American cockroaches taken 1–3 days after adult ecdysis. In mature animals (1–3 months after adult ecdysis) the incorporation rate is strongly depressed, phosphatidylcholine and phosphatidylethanolamine being distinctly more affected than phosphatidylinositol. During 60 min recovery from anaerobiosis only phosphatidylinositol reaches the specific radioactivity found in control muscles. In phosphatidylcholine and phosphatidylethanolamine not even the control rate of labelling is attained during this period. The results are discussed.

Red blood cell age dependent modifications of inositol 1,4,5-trisphosphate

The level of inositol 1,4,5-trisphosphate (Ins1,4,5P3) was determined in human and rabbit red blood cells of different ages. In human erythrocytes, fractionated by discontinuous density gradient centrifugation, Ins1,4,5P3 was 290 nM in the 0.3% low density (youngest) cells compared to values of 107 nM in the whole red blood cell population. A progressive increase in Ins1,4,5P3 was then observed during erythrocyte aging from values of 63 nM in mature erythrocytes to 128 nM in the oldest cells. Determinations of Ins1,4,5P3 in rabbit erythrocytes provided values of 180 nM. Phenylhydrazine was administered to three animals to induce reticulocytosis. Ins1,4,5P3 in rabbit reticulocytes was significantly lower than in the whole red cell population, remained lower in young red blood cells and then increased to normal values during cell maturation. These results provide evidence for an increase of Ins1,4,5P3 during red blood cell aging and could contribute to explain the age-dependent loss of deformability and of Ca2+ homeostasis of these cells.

Immunoexcitotoxicity as the central mechanism of etiopathology and treatment of autism spectrum disorders: A possible role of fluoride and aluminum

Our review suggests that most autism spectrum disorder (ASD) risk factors are connected, either directly or indirectly, to immunoexcitotoxicity. Chronic brain inflammation is known to enhance the sensitivity of glutamate receptors and interfere with glutamate removal from the extraneuronal space, where it can trigger excitotoxicity over a prolonged period. Neuroscience studies have clearly shown that sequential systemic immune stimulation can activate the brains immune system, microglia, and astrocytes, and that with initial immune stimulation, there occurs CNS microglial priming. Children are exposed to such sequential immune stimulation via a growing number of environmental excitotoxins, vaccines, and persistent viral infections. We demonstrate that fluoride and aluminum (Al3+) can exacerbate the pathological problems by worsening excitotoxicity and inflammation. While Al3+ appears among the key suspicious factors of ASD, fluoride is rarely recognized as a causative culprit. A long-term burden of these ubiquitous toxins has several health effects with a striking resemblance to the symptoms of ASD. In addition, their synergistic action in molecules of aluminofluoride complexes can affect cell signaling, neurodevelopment, and CNS functions at several times lower concentrations than either Al3+ or fluoride acting alone. Our review opens the door to a number of new treatment modes that naturally reduce excitotoxicity and microglial priming.