Abstract
The modulatory actions of fluoride on the function of the dihydropyridine-sensitive (L-type) Ca2+ channel were studied in rabbit cardiac myocytes. In cell-attached voltage-clamp experiments, using barium as the charge carrier, fluoride increased the activity of the Ca2+ channel dose-dependently. Low concentrations (<10 mM) of fluoride increased the number of traces with channel activities, and decreased the number of traces without channel activities, resulting in a net increase in the open-channel probability. The effect of 5 mM fluoride on the Ca2+ channel was inhibited by the presence of non-hydrolyzable guanosine diphosphate analog in the cell. On the other hand, high concentrations (>10 mM) of fluoride increased the open-channel duration, resulting in a marked increase in open-channel probability. A pretreatment of myocytes with a phosphatase inhibitor, okadaic acid, virtually abolished the additional effect of fluoride on the open-channel duration or open probability. A concentration of up to 75 mM fluoride had no effect on the Ca2+-channel activity when the myocytes were pretreated with a potent inhibitor of protein kinases, indicating that fluoride increased the Ca2+- channel activity via modulation of the phosphorylation state of the myocyte or the channel protein alone.
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Pathological changes in the tissues of rats (albino) and monkeys (macaca radiata) in fluorine toxicosis
1. Stomach, duodenum, small intestine, kidney, liver, spleen, skin, heart, aorta, lungs, brain, pancreas, adrenals, thyroid and parathyroid of rats and monkeys suffering from chronic fluorosis have been histologically examined. 2. Fluorine has not been found to have any effect on the heart muscle, aorta, skin and parathyroids, whereas it has
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The LD50, excretion and serum and bone levels of F after a high single F and F + Mg dose in rats with findings on cardiac Ca and Mg.
The LD50 for fluoride was elevated from less than 60 mg F/kg body weight to 172 mg F/kg when magnesium (as MgCl2), equivalent to 3 times that of F, was administered by gavage 30 min after the F dose. A dose of 30 mg F/kg elevated the mean steady state
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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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Effects of fluorosis on QT dispersion, heart rate variability and echocardiographic parameters in children - Original Investigation
OBJECTIVE: Chronic fluoride poisoning is called fluorosis. The aim of the study was to investigate effects of fluorosis on cardiovascular system in children by measuring QT dispersion (QTd), corrected QT dispersion (QTcd), heart rate variability (HRV) and echocardiography findings. METHODS: Thirty-five children with dental fluorosis and 26 children as control group
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Trends in urban mortality in relation to fluoridation status.
Mortality trends from 1950 to 1970 were studied for 473 cities in the United States with populations of 25,000 or more in 1950, according to fluoridation status of their water supplies. Findings showed no relationship between fluoridation and observed changes in general mortality over the 20-year period. Also, no relationship
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Fluoride & Myocardial Damage
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Fluoride & Electrocardiogram Abnormalities
An electrocardiogram (ECG) is a diagnostic test that measures the electrical activity of the heart. An ECG can reveal heart rate, heart rhythym (i.e. steady or irregular), and the strength and timing of the heart’s natural electrical signals. ECGs are described in terms of “waves” (e.g. amplitude and duration). Problems
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Fluoride & Arterial Calcification
The major change involved with cardiovascular disease is development of atherosclerosis in critical arteries, which is partially characterized by vascular calcification. The level of coronary artery calcification is thought to be the most important indicator of future cardiovascular events. Increased arterial calcifications have frequently been reported in those with skeletal fluorosis
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