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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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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Delayed fatal hyperkalemia in a patient with acute fluoride intoxication.
A 19-year-old man presented with acute fluoride poisoning. Initially his serum electrolytes were normal, but two hours later he developed ECG evidence of hyperkalemia followed by refractory ventricular fibrillation, suggesting that hyperkalemia may be important in the cardiotoxicity of acute fluoride intoxication. Treatment of fluoride-induced hyperkalemia consists of removal of
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Stimulation of cAMP accumulation in rat aorta and diaphragm by fluorine containing compounds
Evidence is presented that accumulation of cAMP in isolated rat thoracic aorta and diaphragm is stimulated by several fluorine containing compounds (NaF, Na2PO3F (MFP) and SnF2). Time course experiments with NaF showed that maximal stimulation of cAMP accumulation was observed within 2.5 min. NaF and MFP produced significant increases in
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An outbreak of fatal fluoride intoxication in a long-term hemodialysis unit
OBJECTIVE: To determine the cause of an outbreak of acute illness and death in a long-term hemodialysis unit. DESIGN: A retrospective cohort and case-control study of patients receiving hemodialysis and a laboratory study of a model deionization system to purify water for hemodialysis. SETTING: An outpatient hemodialysis unit of a university hospital. PATIENTS:
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Chronic fluoride toxicity and myocardial damage: antioxidant offered protection in second generation rats
This experiment was designed to investigate the extent of peroxidative changes and histological alterations in the myocardium of rats exposed to high fluoride for two generations, in addition to ameliorative role of selenium and vitamin E on the above indices. Adult albino Wistar rats were given fluoride through drinking water
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Fluoride, Blood Pressure and Hypertension
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