Abstract
A study was made of the effects on ovary and uterus of adminis-tering sodium fluoride (10 mg/kg body weight) or aluminium chloride (200 mg/kg body weight) alone and in combination to female albino mice (Mus musculus) for 30 days. The reversibility of the induced effects by withdrawal of NaF + AlCl3 treatment and by administering ascorbic acid (AA), calcium (Ca), or vitamin E alone and in combination were also investigated. All treatments (NaF, AlCl3 , and NaF + AlCl3) resulted in a significant decline of ovarian protein and 3B-and 17B-hydroxysteroid dehydrogenase activities which could be related to increased cholesterol levels in the ovary suggesting altered steroidogenesis. The treatment also caused a hypercholesterolemic effect in serum. Accumulation of glycogen in uterus could be related to inhibition of phosphorylase activity affecting carbohydrate metabolism. The withdrawal of combined treatment for 30 days brought about an incomplete recovery. How-ever, AA, Ca, or vitamin E supplementation alone and in combination produced an additive effect for recovery of most of the parameters almost to con-trol levels. Hence the effects of NaF and/or AlCl3 are transient and reversible.
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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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Management of fluoride induced testicular disorders by calcium and vitamin-E co-administration in the albino rat
Fluoride contamination of drinking water can disrupt male gametogenesis and steroidogenesis and induce testicular oxidative stress. Treatment of rats with sodium fluoride at the dose of 20 mg/kg/day for 28 days resulted in significant diminution of testicular Delta5,3beta-hydroxysteroid dehydrogenase (HSD) and 17beta-hydroxysteroid dehydrogenase (HSD) activities and low plasma levels of
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Beneficial effects of ascorbic acid and calcium on reproductive functions of sodium fluoride-treated prepubertal male rats
The therapeutic effects of ascorbic acid and calcium (Ca2+) supplementation on reproductive functions of fluoride-treated (10 mg/kg body weight) male rats were investigated. Sodium fluoride treatment resulted in a decrease in almost all parameters studied except concentration of testicular cholesterol, which implies that androgen synthesis might not be affected by
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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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Reversal of fluoride-induced alteration in cauda epididymal spermatozoa and fertility impairment in male mice
The effects of sodium fluoride (NaF) ingestion (10 mg NaF/kg body weight) and the possible therapeutic effects of ascorbic acid (AA, 15 mg/animal/day) and/or calcium phosphate (Ca, 25 mg/animal/day) on the reproductive functions and fertility of male mice were investigated. NaF-ingestion brought about a significant decline in sperm acrosomal acrosin
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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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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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Mayo Clinic: Fluoridation & Bone Disease in Renal Patients
The available evidence suggests that some patients wtih long-term renal failure are being affected by drinking water with as little as 2 ppm fluoride. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers. The finding of adverse effects in patients drinking water with 2 ppm of fluoride suggests that a few similar cases may be found in patients imbibing 1 ppm, especially if large volumes are consumed, or in heavy tea drinkers and if fluoride is indeed the cause. It would seem prudent, therefore, to monitor the fluoride intake of patients with renal failure living in high fluoride areas.
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Unheeded Warnings: Government Health Authorities Ignore Fluoride Risk for Kidney Patients
Despite the well known fact that individuals with kidney disease are at much higher risk of fluoride toxicity than the general population, there has yet to be any attempt in the United States, or any other country that practices mass-scale water fluoridation to determine the prevalence of fluoride-related effects (e.g.,
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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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