Abstract
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 the cell viability, intracellular reactive oxygen species (ROS) level, the changes of mitochondrial membrane potential, and the cell apoptosis. Sodium fluoride (NaF) at concentrations of 0, 2, 4, 8, and 16 mg/L was administered to cultured H9c2 cells for up to 48 h. After the treatment, H9c2 cells were collected and the associated parameters were measured by flow cytometry. Our study found that fluoride not only inhibited H9c2 cell proliferation but also induced cell apoptosis. With the increment of NaF concentration, the apoptotic rates and ROS generation were increased, while the [mitochondrial membrane potential] was decreased. In summary, these data suggested that NaF-induced H9c2 cell apoptosis is mediated by direct increased intracellular ROS and downregulated [mitochondrial membrane potential].
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Epigallocatechin gallate potentially attenuates fluoride induced oxidative stress mediated cardiotoxicity and dyslipidemia in rats
The present study was undertaken to evaluate the cardioprotective role of (-)-epigallocatechin-gallate (EGCG) against Fluoride (F) induced oxidative stress mediated cardiotoxicity in rats. The animals exposed to F as sodium Fluoride (NaF) (25mg/kg BW) for 4 weeks exhibited a significant increase in the levels of cardiac troponins T and I
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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-induced oxidative stress in rat myocardium through the Bax/Bcl-2 signalling pathway
The purpose of this study was to investigate whether fluoride (F) induces cardiotoxicity in rats and to discuss its underlying mechanisms by detecting morphological change, enzyme activity of oxidative stress, and the expression of Bcl-2 family protein. With increasing dosages of F, obvious pathological changes occurred in the myocardial tissue
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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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Single oral acute fluoride exposure causes changes in cardiac expression of oxidant and antioxidant enzymes, apoptotic and necrotic markers in male rats
Several studies have shown that acute fluoride (F-) exposure impairs cardiac function, but the molecular mechanism is not clear. In order to study this, male Wistar rats were treated with single oral doses of 45 and 90 mg/kg F- for 24 h. A significant accumulation of F- was found in the serum
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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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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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Fluoride, Blood Pressure and Hypertension
Individuals with blood pressure readings that exceed 140/90 are considered hypertensive. Hypertension can increase the risk of stroke, heart attack, heart failure, aortic aneurysms, and peripheral arterial disease. An association between increased fluoride in ground water and increased prevalence of hypertension has been observed, especially among adult males (Amini et
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Fluoride content in tea and its relationship with tea quality.
J Agric Food Chem. 2004 Jul 14;52(14):4472-6. Fluoride content in tea and its relationship with tea quality. Lu Y, Guo WF, Yang XQ. Department of Tea Science, Zhejiang University, 268 Kaixuan Road, Hangzhou 310027, People's Republic of China. Abstract: The tea plant is known as a fluorine accumulator. Fluoride (F) content in fresh leaves collected
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Nutrient Deficiencies Enhance Fluoride Toxicity
It has been known since the 1930s that poor nutrition enhances the toxicity of fluoride. As discussed below, nutrient deficiencies have been specifically linked to increased susceptibility to fluoride-induced tooth damage (dental fluorosis), bone damage (osteomalacia), neurotoxicity (reduced intelligence), and mutagenicity. The nutrients of primary importance appear to be calcium,
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