Abstract
Previous work has shown that a high fluoride intake in rodents leads to histopathological changes in the germinal epithelium of testes that is associated with zinc deficiency. The purpose of this study was to determine whether supplemental dietary Zn would protect against testicular toxicity induced by fluoride in a small rodent, the bank vole. The 4-month exposure period to fluoride (200 g/ml of drinking water) induced histopathological changes (hemorrhage in interstitium, necrosis and apoptosis in seminiferous tubule epithelium) which were accompanied by decreased testicular zinc concentration and increased lipid peroxidation. Supplemental dietary zinc (110–120 g/g) together with fluoride treatment resulted in complete reversal of the fluoride-mediated effects. However, supplemented dietary Zn did not affect the accumulation of fluoride in the testes and bone. These data suggest that a zinc-enriched diet protects seminiferous tubules against fluoride toxicity by preventing the fluoride-induced testicular zinc deprivation.
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N-acetylcysteine alleviates fluoride-induced testicular apoptosis by modulating IRE1?/JNK signaling and nuclear Nrf2 activation.
Highlights NaF exposure triggered testicular apoptosis and sex hormonal disruption. NaF exposure increased the expression of ER stress mediators in testis of rat. NAC pretreatment attenuated IRE1?-JNK-mediated apoptosis induced by NaF. The alteration of Nrf2-dependent redox homeostasis was involved in the protective effect of NAC against NaF-induced testicular apoptosis. We previously
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[Study on antagonistic effects of selenite on fluoride-induced impairments of testis and epididymis in rats].
Objective: To study the mechanisms of the antagonistic action of selenite on fluoride-induced male reproductive damages, and find out the optimal level of selenite in drinking water against fluoride toxicity. Methods: Five groups of SD male rats were provided with deionized drinking water containing 0 and 150 mg/L NaF, and
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The effect of high fluoride intake on tissue trace elements and histology of testicular tubules in the rat
1. Male Wistar rats were exposed to fluoride (F) at concentrations of 100- and 200 ppm in their drinking water for 6- and 16 weeks. 2. The high F intake caused several-fold increase in the F concentrations in the testes and bone as compared with control rats, both after the
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Fluoride toxicity in the male reproductive system
This review covers the current scientific understanding of the links between environmental exposure to fluoride (F) and its known or potential effects on human male fertility. The most important consequences of these F exposures are: changes in the structure and functional behavior of spermatozoa, disruption of spermatogenesis, and disturbances of
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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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Fluoride & Oxidative Stress
A vast body of research demonstrates that fluoride exposure increases oxidative stress. Based on this research, it is believed that fluoride-induced oxidative stress is a key mechanism underlying the various toxic effects associated with fluoride exposure. It is also well established that fluoride's toxic effects can be ameliorated by exposure
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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 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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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 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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