Abstract
Effects of sodium fluoride (NaF) (30 mg kg-1 body weight) and ascorbic acid ingestion along with sodium fluoride for 30 days each were studied to evaluate its possible role as an ameliorative agent on functions of reproductive organs and spermatozoa of the fluorotic guinea pig. The cauda epididymal spermatozoa were highly sensitive to the effects of sodium fluoride as their structural and metabolic alterations led to marked decreases in their motility, live:dead ratio and sperm mitochondrial activity index but increases in sperm abnormalities and alterations in sperm membrane phospholipids, particularly phosphatidylinositol and phosphatidyl serine. The activities of ATPase and succinate dehydrogenase as well as glutathione levels were decreased in testis by sodium fluoride treatment, revealing disturbances in its metabolism. However, testicular cholesterol was not affected. Ingestion of ascorbic acid led to the enhancement in the levels of these parameters almost to control levels. These results reveal the ameliorative role of ascorbic acid in mitigation of fluoride-induced toxicity on guinea pig sperm structure and metabolism.
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[The primary study of antagonism of selenium on fluoride-induced reproductive toxicity of male rat].
The protective effect of ascorbic acid at dose level of 1.0 mg/L in drinking water against the fluoride-induced damage on reproductive system of rat was studied. 150 mg/L sodium fluoride (NaF) in drinking water of male rat can cause the significant decrease of sperm count and mobility, the increase of
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Vitamin C and E supplementation can ameliorate NaF mediated testicular and spermatozoal DNA damages in adult Wistar rats.
Objective: Present study was designed to explore the efficacy of vitamin C and E (VC&VE) against fluoride mediated testicular, epididymal and spermatozoal anomalies. Materials and methods: Thirty two adult Wistar rats were divided into four groups. Group-I was control; Group-II received sodium fluoride (NaF) at 15 mg/kg/day
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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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Fluoride and aluminum induced toxicity in mice epididymis and its mitigation by vitamin C
Treatment of adult male mice with sodium fluoride (NaF, 10 mg/kg bw/day) and aluminium chloride (AlCl3, 200 mg/kg bw/day) simultaneously for 30 days caused marked histological changes in the epididymis accompanied by decreased levels of protein and sialic acid and also lowered activities of adenosine triphosphatase (ATPase) and succinate dehydrogenase
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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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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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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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Fluoride Is Not an Essential Nutrient
In the 1950s, dentists believed that fluoride was a “nutrient.” A nutrient is a vitamin or mineral that is necessary for good health. Dentists believed that fluoride ingestion during childhood was necessary for strong, healthy teeth. A “fluoride deficiency” was thus believed to cause cavities, just like a deficiency of calcium can
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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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