Abstract
Acute fluoride intoxication increases intracellular calcium (Cai), manifested by increased twitch tension in cardiac muscle, and by potassium efflux (mediated by Ca2+-dependent K+ channels) in fluoridated erythrocytes. Fluoride, like isoproterenol, stimulates adenylate cyclase, and could increase Cai via the effects of cAMP on Ca2+ channels. However, while the inotropic effects of fluoride mimicked isoproterenol in rat atria, their effects on the time course of isometric contraction were quite different. In addition, acetylcholine negated isoproterenol’s effect on twitch tension but did not modulate the effects of fluoride. Further, the Ca2+ channel antagonist verapamil had no effect on fluoride-stimulated K+ efflux from erythrocytes. Fluoride also inhibits Na+-K+ ATPase, and increases intracellular Na+, so could increase Cai via Na+-Ca2+ exchange. Lanthanum, which blocks Na+-Ca2+ exchange, blocks fluoride-induced K+ efflux in erythrocytes. We conclude that the effects of fluoride on adenylate cyclase are not important in intact tissue, and that inhibition of Na+-K+ ATPase and subsequent Na2+-Ca2+ exchange may be the mechanism of increased Cai in acute fluoride toxicity.
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The effects of fluoridated water on rat urine and tissue cAMP levels
Male Wistar rats were fed a fluoride deficient diet (less than 0.5 parts/10(6) F), and either distilled water or fluoridated water (1.0 parts/10(6)). By week 3, the control group had urinary excretions of 106 +/- 5 nmol cAMP/day (mean +/- SEM) whereas the experimental group excreted 129 +/- 6 nmol
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Sodium fluoride induces apoptosis in H9c2 cardiomyocytes by altering mitochondrial membrane potential and intracellular ROS level
Chronic excessive fluoride intake is known to be toxic, and effects of long-term fluorosis on different organ systems have been examined. However, there are few studies about the effects of fluorosis on cardiovascular systems. Here, we studied the fluoride-induced apoptosis in H9c2 cells and determined the underlying molecular mechanisms including
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Fluoride Exposure Induces Inhibition of Sodium-and Potassium-Activated Adenosine Triphosphatase (Na+, K+-ATPase) Enzyme Activity: Molecular Mechanisms and Implications for Public Health.
In this study, several lines of evidence are provided to show that Na+ , K+ -ATPase activity exerts vital roles in normal brain development and function and that loss of enzyme activity is implicated in neurodevelopmental, neuropsychiatric and neurodegenerative disorders, as well as increased risk of cancer, metabolic, pulmonary and
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Fluoride induces apoptosis in H9c2 cardiomyocytes via the mitochondrial pathway.
Highlights We studied the toxic effects of different concentrations of NaF in H9c2 cells. NaF inhibited H9c2 cell proliferation and induced early apoptosis. Mitochondrial membrane potential decreased with increase in NaF. Caspase-3, caspase-9, and cytochrome c mRNA levels increased with increase in NaF. Fluoride induces apoptosis via activation of the
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Rutin potentially attenuates fluoride induced oxidative stress mediated cardiotoxicity, blood toxicity and dyslipidemia in rats
The present study was undertaken to evaluate cardio protective effect of rutin against sodium fluoride-induced oxidative stress mediated cardio toxicity and blood toxicity. Cardiac injury was induced by daily administration of sodium fluoride 600ppm in distilled water for 4 weeks. The animals exposed to NaF exhibited a significant increase in
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