Abstract
Selective low (15 mg sodium fluoride (NaF)/L) and relatively high (150 mg NaF/L) doses of in vivo fluoride (F) treatment to Swiss albino mice through drinking water elicited organ-specific toxicological response. All the F-exposed groups showed severe alterations in both liver and kidney architectures, but there was no significant change in the rate of water consumption and body weight. Vacuolar degeneration, micronecrotic foci in the hepatocytes, and hepatocellular hypertrophy were evident in the mice exposed to low dose (15 mg NaF/L for 30 days) while sinusoidal dilation with enlarged central vein surrounded by deep-blue erythrocytes were preponderant when treated with the same dose for a period of 90 days. Blood filled spaces, disintegration of tubular epithelium, and atrophy of glomeruli were also recorded in the kidney of the same treatment group. Change in reduced glutathione level (GSH), glutathione-s-transferase (GST) activity, malondialdehyde (MDA) production in both liver and kidney, disturbances in liver function, induction of heat shock protein 70 (Hsp 70) expression in kidney and its down regulation in liver were positively correlated with histopathological lesion.
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Changes in fluoride levels in the liver, kidney, and brain and in neurotransmitters of mice after subacute administration of fluoride
The effects of fluoride after subacute oral administration of NaF at levels of 0, 1, 5, 25, and 125 ppm F– were evaluated in adult male BALB/c mice. Fluoride levels in the murine liver, kidney, and cerebrum after one month were determined using a highly sensitive flow-injection apparatus with a
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Fluoride in drinking water exacerbates glomerulonephritis and induces liver damage in ICR-derived glomerulonephritis mice
To evaluate the effects of fluoride on the kidney and the liver of ICR-derived glomerulonephritis (ICGN) mice by using laboratory tests and pathological examinations, fluoride was administered to the ICGN mice at 0, 25, 50, 100, and 150 ppm in drinking water for 4 weeks and to the ICR mice,
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Histologic findings in the kidney, liver, pancreas, adrenal, and thyroid glands of the rat following sodium fluoride administration
1. Fluoride toxicosis was induced in young rats of the Long-Evans strain. Ten rats received a total of 406.47 mg. each of sodium fluoride injected intraperitoneally over a fifteen-day period, to induce acute poisoning. Seven rats survived, of which six were analyzed for this study. Ten others received a total
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Maize purple plant pigment protects against fluoride-induced oxidative damage of liver and kidney in rats
Anthocyanins are polyphenols and well known for their biological antioxidative benefits. Maize purple plant pigment (MPPP) extracted and separated from maize purple plant is rich in anthocyanins. In the present study, MPPP was used to alleviate the adverse effects generated by fluoride on liver and kidney in rats. The results
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Fluoride exposure and kidney and liver function among adolescents in the United States: NHANES, 2013–2016.
Highlights Plasma fluoride concentrations are associated with kidney and liver parameters among United States (U.S.) adolescents Higher water fluoride concentrations are associated with lower blood urea nitrogen among U.S. adolescents Fluoride exposure may contribute to complex changes in kidney and liver related parameters among U.S. adolescents Altered kidney and/or liver
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Fluoride as a Cause of Kidney Disease in Animals
Because the kidney is exposed to higher concentrations of fluoride than all other soft tissues (with the exception of the pineal gland), there is concern that excess fluoride exposure may contribute to kidney disease - thus initiating a "vicious cycle" where the damaged kidneys increase the accumulation of fluoride, causing in
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Fluoride as a Cause of Kidney Disease in Humans
Because the kidney is exposed to higher concentrations of fluoride than all other soft tissues (with the exception of the pineal gland), there is concern that excess fluoride exposure may contribute to kidney disease - thus initiating a "vicious cycle" where the damaged kidneys increase the accumulation of fluoride, causing
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Fluoridation of drinking water and chronic kidney disease: Absence of evidence is not evidence of absence
A fairly substantial body of research indicates that patients with chronic renal insufficiency are at an increased risk of chronic fluoride toxicity. Patients with reduced glomerular filtration rates have a decreased ability to excrete fluoride in the urine. These patients may develop skeletal fluorosis even at 1 ppm fluoride in the drinking water.
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Fluoride Gels & Kidney Function
Scientists have found that the application of "Fluoride Gels" at the dental office causes very high spikes in the blood fluoride level. The high spikes in blood fluoride levels are a result of three factors: the high concentration of fluoride in the gel (= 12.3 mg of fluoride in each
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