Abstract
The aim of this study was to examine the influence of vitamin E on the liver morphology and carbohydrate enzyme activities of rats intoxicated with sodium fluoride (NaF). Eighteen adult male Wistar rats on a standard rat diet were divided into three equal groups for a five-week experiment: a control group on distilled water; an experimental group I dosed with 4 mg NaF/rat/24hr in the drinking water; and a group II with the same dose of NaF plus 3 mg vitamin E/rat/24hr. Pathomorphological changes in the liver were assessed by paraffin histopathology, and changes in protein content and carbohydrate enzyme activities of aldolase, malate dehydrogenase, lactate dehydrogenase, and sorbitol dehydrogenase were determined by standard methods. Under conditions of this study with rats, supplemental vitamin E partially but did not completely prevent the toxic effects of NaF on the liver histopathology and carbohydrate enzyme activities.
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Induction of oxidative stress on reproductive and metabolic organs in sodium fluoride-treated male albino rats: protective effect of testosterone and vitamin E coadministration
The present study was undertaken to search out the effect of sodium fluoride, a water pollutant noted throughout the world, including India, on oxidative stress induction in reproductive tissues, sperm pellet, and metabolic tissues like the liver and kidney. The protective effects of testosterone or vitamin-E coadministration were also observed
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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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[The influence of methionine and vitamin E on oxidative stress in rats’ liver exposed to sodium fluoride]
BACKGROUND: Fluorine influences many processes occurring in the organism. Controversies over the evaluation of the biological effects of this substance are due to a small difference between tolerable and toxic fluorine doses. One of the main mechanisms of the fluorine toxic action is its ability to induce oxidative stress via
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Lipid peroxidation in fluorosis and the protective role of dietary factors
The influence of chronic Fl intoxication on lipid peroxidation and the state of the antioxidant system was studied in rats on different diets. Chronic Fl intoxication inhibited antioxidant activity and caused an increase in the rate of peroxidation and the level of lipoperoxides in liver, brain and serum. Diets with
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Fetotoxicity of fluoride in rats and the protective action of some antioxidants
The aim of this study was to assess the efficacy of antioxidants to prevent or alleviate fluoride (F) toxicity in pregnant female Wistar rats and their fetuses. Groups of pregnant rats (10 in each group) were treated by oral intubation with F (40 mg F – /kg bw/day from NaF),
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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 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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Fluoridation of drinking water and chronic kidney disease: Absence of evidence is not evidence of absence
A fairly substantial body of research indicates that patients with chronic renal insufficiency are at an increased risk of chronic fluoride toxicity. Patients with reduced glomerular filtration rates have a decreased ability to excrete fluoride in the urine. These patients may develop skeletal fluorosis even at 1 ppm fluoride in the drinking water.
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Kidney Patients Are at Increased Risk of Fluoride Poisoning
It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients
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Dental Fluorosis & Enamel Hypoplasia in Children with Kidney Disease
Children with kidney disease are known to have high levels of fluoride in their blood and to be at risk for disfiguring tooth defects. Research suggests that high levels of fluoride in blood, which can cause the tooth defect known as dental fluorosis, can contribute to the defects that occur
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