Abstract
Chronic exposure of humans to fluorine compounds in the air, water and food may be atherogenic via the activation of oxidative stress and increased ROS production. The most important factor that promotes the formation of ROS seems to be the oxidoreduction of electron carriers in the critical points of the respiratory chain, which depends, among other things, on the cellular demand for ATP. This paper examines the effect of fluorides in concentrations determined in human serum on the intracellular synthesis of ROS, the activity of the respiratory chain enzymes and the synthesis of ATP via oxidative and substrate-level phosphorylation. The incubation of macrophages in fluoride solutions significantly decreased the amount of synthesized cellular ATP and increased formation of ROS and apoptosis in a dose-dependent pattern. The addition of respiratory chain inhibitors resulted in a significant decrease in the synthesized ROS. Sodium fluoride probably promotes oxidative stress in macrophages, which is manifested by a strong increase in ROS synthesis and a decrease in ATP. We suppose that fluoride may destabilize the action of respiratory chain. Our results indicate that the respiratory chain is the main site of ROS synthesis. One cannot exclude the stimulating role of fluorine compounds on the formation of ROS that is independent of the respiratory chain.
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Fluoride and generation of pro-inflammatory factors in human macrophages
Fluorosis from excessive exposure to fluoride can result in inflammatory reactions involving macrophages and their differentiation, a process that is rapidly followed by generation of prostanoids—products of arachidonic acid metabolism, including the pro-inflammatory factors prostaglandin PGE2 and thromboxane TXA2, which are implicated in atherogenesis and rapidly increase during acute inflammation. This paper examines the effect
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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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Observations of two-dimensional (2D) echocardiograms in patients with fluorine-associated aortic sclerosis
Forty-six patients with endemic fluorosis were assigned to 4 subgroups based on their age and then received echocardiograms that were compared with echocardiograms of 46 healthy cases in a region affected by fluorosis and 46 healthy cases in a region unaffected by fluorosis via observations; a preliminary exploration was made
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Assessment of relationship on excess fluoride intake from drinking water and carotid atherosclerosis development in adults in fluoride endemic areas, China.
Cross-sectional analysis was conducted to access the relationships between developing carotid artery atherosclerosis through consuming high fluoride in drinking water and its possible mechanism, using the baseline data collected from 585 study subjects. In the cross sectional analysis, subjects were divided into four groups based on the concentrations of fluoride
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Oxidative indices correlate with dyslipidemia and pro-inflammatory cytokine levels in fluoride-exposed rats
The aim of this study was to establish the effects of fluoride on lipid metabolism and attendant inflammatory response by exposing rats to 50 mg L-1 and 100 mg L-1 of fluoride through drinking water for seven weeks. Both concentrations led to hypercholesterolemia while the 100 mg L-1 concentration induced
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Fluoride & Arteriosclerosis
Healthy arteries are flexible and elastic, allowing efficient transfer of blood and nutrients from the heart to the rest of the body. Arteriosclerosis refers to a stiffening of the arteries, including loss of elasticity. This is a slow, progressive disease that may begin early in life from damage to the
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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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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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Fluoride & Myocardial Damage
Structural damage to the heart resulting from fluoride toxicity has been observed in numerous human and animal studies. The general features of this damage include cloudy swelling, vacuolization or vacuolar degeneration, hemorrhages, interstitial edema, fibrous necrosis, dissolution of nuclei, and thickening of the vessel walls in the heart muscle (Basha
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