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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Reversal of fluoride induced cell injury through elimination of fluoride and consumption of diet rich in essential nutrients and antioxidants
The objective of the present communication is to address the issues concerning reversal of fluoride induced cell injury and disease (i.e. fluorosis) through the elimination of fluoride and consumption of a diet containing essential nutrients and antioxidants. Humans afflicted with fluorosis, as a result of consuming fluoride contaminated water or
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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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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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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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Fluoridated Water Causes Severe Dental Fluorosis in Children with Diabetes Insipidus
This section on Diabetes includes: • Fluoride & Impaired Glucose Tolerance • Fluoride & Insulin • Fluoride Sensitivity Among Diabetics • Fluoridated Water Causes Severe Dental Fluorosis in Children with Diabetes Insipidus • NRC (2006): Fluoride’s Effect on Glucose Metabolism Excessive exposure to fluoride causes a defect of the tooth enamel known as dental fluorosis. In
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Fluoride Exposure Increases Metabolic Requirement for Magnesium
Fluoride's toxicity is significantly enhanced in the presence of nutritional deficiencies. Similarly, fluoride exposure increases the body's requirement for certain nutrients. An individual with a high intake of fluoride, for example, will need a proportional increase in calcium to avoid the mineralization defects (e.g., osteomalacia) that fluoride causes to bone
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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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Fluoride & Rickets
One of fluoride's most well-defined effects on bone tissue is it's ability to increase the osteoid (unmineralized bone) content of bone. When bones have too much osteoid, they become soft and prone to fracture -- a condition known as osteomalacia. When osteomalacia develops during childhood, it is called "rickets." The potential for fluoride
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