Abstract
We have evaluated the ameliorative effect of vitamin D on fluoride-induced embryotoxicity in pregnant rats. Oral administration of sodium fluoride (NaF; 40 mg/kg body weight) from days 6 to 19 of gestation caused, as compared with control, significantly lowered body weight, feed consumption, absolute uterine weight and number of implantations. As compared with the control, higher incidence of skeletal (presence of wavy ribs, 14th rib, dumbbell-shaped 5th sternebrae, incomplete ossification of skull) and visceral (subcutaneous haemorrhage) abnormalities was recorded in the foetuses of fluoride-treated pregnant rat. Vitamin D (2 ng/0.2 ml olive oil/animal/day po) treatment significantly ameliorated the fluoride-induced reductions in body weight, feed consumption and absolute uterine weight. As compared with fluoride-treated alone, the total percentage of skeletal and visceral abnormalities observed in foetuses was significantly lowered in fluoride plus vitamin D-treated animals. These findings suggest that vitamin D treatment significantly reduced the severity and incidence of fluoride-induced embryotoxicity. The ameliorative effect of vitamin D against skeletal and visceral abnormalities could be due to stimulation of intestinal absorption of calcium and phosphate, thus raising the plasma calcium and phosphate concentrations.
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Amelioration of fluoride toxicity by vitamins and calcium on reproductive organs of female rat
Normal female rats of Wistar strain (Rattus norvegicus) weighing between 150–200 g were treated with fluoride (Fl) contaminated drinking water (FW, 5.8 ppm), vitamin C (6 mg) and vitamin C (6 mg) + D (6 mg once a week) + calcium (6 mg) for 30 days. Fl water treatment to
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Amelioration of fluoride toxicity by vitamin E and D in reproductive functions of male mice
Studies on the beneficial effects of vitamins E and D supplementation on functions of caput and cauda epididymides, their spermatozoa, vas deferens and seminal vesicle of sodium fluoride (NaF) treated (10 mg/kg body weight) male mice (Mus musculus) were carried out. The NaF treatment resulted in significant decrease in the
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Amelioration of fluoride toxicity in rats through vitamins (C, D) and calcium
The healthy, adult male rats (Rattus norvegicus) were treated with fluoride water (F.W.+5.8 ppm), F.W.+ ascorbic acid and F.W. + vitamins (C, D) and Ca+2 for 60 days. Fluoride water ingestion to rats for 60 days resulted in significant reduction of seminal vesicle weight, sperm motility and sperm density of
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Mitigating effects of some antidotes on fluoride and arsenic induced free radical toxicity in mice ovary
The effects of oral administration of sodium fluoride (NaF) and/or arsenic trioxide (As(2)O(3)) (5 mg and 0.5 mg/kg body weight, respectively) for 30 days were investigated on free radical induced toxicity in the mouse ovary. The reversibility of the induced effects after withdrawal of NaF+As(2)O(3) treatment and by administration of
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Selenium may suppress peripheral blood mononuclear cell apoptosis by modulating HSP70 and regulate levels of SIRT1 through reproductive hormone secretion and oxidant stress in women suffering fluorosis.
Excessive taking fluoride (F) causes severe damage to reproductive system through stimulation of apoptosis and oxidant stress. Selenium (Se) may promote anti-oxidant enzymes and invert cell apoptosis. The aim of this study was to investigate the effect of Se on peripheral blood mononuclear cell (PBMC) apoptosis and oxidant stress in
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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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Skeletal Fluorosis & Individual Variability
One of the common fallacies in the research on skeletal fluorosis is the notion that there is a uniform level of fluoride that is safe for everyone in the population. These "safety thresholds" have been expressed in terms of (a) bone fluoride content, (b) daily dose, (c) water fluoride level, (d) urinary fluoride level, and (e) blood fluoride level. The central fallacy with each of these alleged safety thresholds, however, is that they ignore the wide range of individual susceptibility in how people respond to toxic substances, including fluoride.
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Fluoride Exposure Increases Metabolic Requirement for Calcium & Vitamin D
It is well known that individuals with nutrient deficiencies are more susceptible to fluoride toxicity, including fluoride's bone effects. As discussed in the following studies, fluoride increases the skeleton's need for calcium (and vitamin D) by increasing the amount of unmineralized tissue (osteoid) in the bone. When insufficient calcium and
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Factors which increase the risk for skeletal fluorosis
The risk for developing skeletal fluorosis, and the course the disease will take, is not solely dependent on the dose of fluoride ingested. Indeed, people exposed to similar doses of fluoride may experience markedly different effects. While the wide range in individual response to fluoride is not yet fully understood, the following are some of the factors that are believed to play a role.
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Fluoride Exposure Aggravates the Impact of Iodine Deficiency
A consistent body of animal and human research shows that fluoride exposure worsens the impact of an iodine deficiency. Iodine is the basic building block of the T3 and T4 hormones and thus an adequate iodine intake is essential for the proper functioning of the thyroid gland. When iodine intake is inadequate during infancy and
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