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.
-
-
[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
-
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
-
[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
-
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
-
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
Related Studies :
-
-
-
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,
-
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
-
Fluoride's Effect on Male Reproductive System -- The "Sprando/Collins" Anomaly
In contrast to the findings of over 60 animal studies from other research teams, a series of studies by FDA researchers Sprando & Collins reported virtually no evidence of reproductive toxicity among animals treated with very high levels of fluoride exposure. The reasons for this discrepancy remains unclear. Excerpts from Sprando/Collins' Studies: "This study
-
Fluoride's Effect on the Male Reproductive System -- In Vitro Studies
Carefully controlled in vitro studies have found that direct exposure of fluoride to the testes or semen inhibits testosterone production and damages sperm. While researchers have known since the 1930s that mega concentrations of fluoride can completely (but reversibly) immobilize sperm, it was not until the 1970s and 1980s that researchers found that relatively modest concentrations of fluoride could cause damage prior to complete immobilization.
-
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
Related FAN Content :
-