SUMMARY: As part of our investigation of fluoride toxicity effects in a group of 80
Swiss albino adult male mice, we examined the mitigating effects of black tea extract
(BTE) on the F-induced enzymatic and non-enzymatic parameters of oxidative stress
in the cerebral hemisphere (CH), cerebellum (CB), and medulla oblongata (MO) of the brains of these mice. Oral administration of 6 and 12 mg NaF/kg bw/day to the mice for 30 days resulted in a significant increase in level of lipid peroxidation (LPO) and dehydroascorbic (DAA) acid as well as a decrease in glutathione (GSH), total
ascorbic acid (TAA), and reduced ascorbic acid. In addition, the activities of the
enzymatic antioxidants catalase (CAT), superoxide dismutase (SOD), glutathione
reductase (GSH-Pr), and glutathione peroxidase (GSH-Px) as well as cholinesterase
(ChE) also decreased. No significant recovery in any of these parameters was
observed upon withdrawal of the NaF treatment for 30 days. However, administration of BTE along with the NaF during the experiment resulted in significant mitigation of all the NaF-induced effects that were examined.
Public-health risks from tea drinking: Fluoride exposure.
Aims: Due to new evidence on fluoride neurotoxicity during early life, this study examined maternal exposure to fluoride through tea consumption in a low-fluoride region and measured fluoride releases from commercially available teas (tea bags and loose teas) to determine the need to limit fluoride exposure. Methods:
Mitigation of sodium fluoride induced toxicity in mice brain by black tea infusion.
SUMMARY: In an extension of previous work on fluoride (F) toxicity in a group of 80 Swiss albino mice, the mitigating effects of polyphenols in black tea on the F-induced increase in glycogen, cholesterol, and total lipids in the cerebral hemisphere (CH), cerebellum (CB), and medulla oblongata (MO) regions of
Amelioration by black tea of sodium fluoride-induced changes in protein content of cerebral hemisphere, cerebellum and medulla oblongata in brain region of mice.
Oral administration of sodium fluoride (NaF, 6 and 12 mg/kg body weight/day) to Swiss strain male albino mice for 30 days caused significant dose-dependant reduction in the content of acidic, basic, neutral, and total protein in cerebral hemisphere, cerebellum and medulla oblongata region of brain. After 30 days of NaF
Non-Endemic Skeletal Fluorosis: Causes And Associated Secondary Hyperparathyroidism (Case Report and Literature Review).
Highlights Fluorocarbon “huffing” is an under-appreciated cause of skeletal fluorosis (SF) We present a SF case with hyperparathyroidism, osteosclerosis, and osteomalacia SF may go undetected due to variation in symptoms, radiology, and biochemistry Dietary calcium, prior bone health, and skeletal F exposure influence SF features SF is common in
Effect of excessive green tea versus fluoride and caffeine on body weight and serum thyroid hormones in male mice
Green tea is a worldwide used beverage rich in fluoride and caffeine. To study the effect of excessive green tea intake versus fluoride and caffeine on body weight and serum thyroid hormones in male mice. Also, to confirm the effect of excessive green tea intake on thyroid gland was due
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Fluoride's Direct Effects on Brain: Animal Studies
The possibility that fluoride ingestion may impair intelligence and other indices of neurological function is supported by a vast body of animal research, including over 40 studies that have investigated fluoride's effects on brain quality in animals. As discussed by the National Research Council, the studies have consistently demonstrated that fluoride, at widely varying concentrations, is toxic to the brain.
Fluoride: Developmental Neurotoxicity.
Developmental Neurotoxicity There has been a tremendous amount of research done on the association of exposure to fluoride with developmental neurotoxicity. There are over 60 studies reporting reduced IQ in children and several on the impaired learning/memory in animals. And there are studies which link fluoride to Attention Deficit Hyperactivity Disorder. Teaching
Exposure Pathways Linked to Skeletal Fluorosis
Excessive fluoride exposure from any source -- and from all sources combined -- can cause skeletal fluorosis. Some exposure pathways , however, have been specifically identified as placing individuals at risk of skeletal fluorosis. These exposure pathways include: Fluoridated Water for Kidney Patients Excessive Tea Consumption High-Fluoride Well Water Industrial Fluoride Exposure Fluorinated Pharmaceuticals (Voriconazole
Estimated "Threshold" Doses for Skeletal Fluorosis
For over 40 years health authorities stated that in order to develop crippling skeletal fluorosis, one would need to ingest between 20 and 80 mg of fluoride per day for at least 10 or 20 years. This belief, however, which played an instrumental role in shaping current fluoride policies, is now acknowledged by the National Academy of Sciences (NAS) and other US health authorities to be incorrect.
Skeletal Fluorosis in the U.S.
Although there has been a notable absence of systematic studies on skeletal fluorosis in the U.S., the available evidence indicates that the consumption of artificially fluoridated water is likely to cause skeletal fluorosis and other forms of bone disease in people with kidney disease and other vulnerable populations.
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