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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Effective interventional approach to control anaemia in pregnant women
Anaemia in pregnancy and low birth weight babies, a serious public health problem, troubles India and several other nations. This article reports the results of a approach to address the issue. Women up to 20 week pregnancy with haemoglobin (Hb) 9.0 g/dl or less, those with urinary fluoride beyond 1.0
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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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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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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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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 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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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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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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