Abstract

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 6- and 16 wk exposure; the bone F, but not testicular F, appeared to increase with dose and time. 3. F exposure (100- and 200 ppm) decreased significantly the concentrations of zinc (Zn) in the testes, plasma, liver and kidneys particularly in the 16 wk groups; in the bone Zn tended to increase, however. 4. The iron concentrations of the testes and plasma were not affected by F, whereas those of the liver, kidneys and bone appeared to increase under the influence of F. 5. The concentrations of copper and manganese in the testes, liver and kidneys were not changed by F exposure. 6. Fifty percent of the 100- and 200 ppm F rats after 16 weeks exhibited histopathologic changes in the germinal epithelium of the testes, which resembled those in Zn-deficient rats. 7. The data suggest that a deprivation of testicular Zn due to a high F intake may be directly responsible for the injury of testicular tubules.

• Related Studies :

  • 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

  • Protective effects of blackberry and quercetin on sodium fluoride-induced oxidative stress and histological changes in the hepatic, renal, testis and brain tissue of male rat

    BACKGROUND: Sodium fluoride (NaF) intoxication is associated with oxidative stress and altered antioxidant defense mechanism. The present study was carried out to evaluate the potential protective role of blackberry and quercetin (Q) against NaF-induced oxidative stress and histological changes in liver, kidney, testis and brain tissues of rats. METHODS: The rats

  • Influence of supplementary vitamins and minerals on lipid peroxidation and redox state in heart, kidney and liver of rats exposed to fluoride.

    The effect of fluoride (F) and supplementary vitamins and minerals on lipid peroxidation (LPO) and redox state (RS) in heart , kidney and liver of 40 (4 groups of 10) male Wistar rats were studied. One group of rats was left untreated as control, group 1 was received 5 mg/l

  • Evaluation of the toxicity of fluorine in Antarctic krill on soft tissues of Wistar rats

    Antarctic krill are a potential food source for humans and animals, but krill are known to contain high levels of fluorine (F). In this study, we investigated the toxicity of F in Antarctic krill using Wistar rats. There were three experimental groups: The control group were fed a basal diet,

  • Zinc protection from fluoride-induced testicular injury in the bank vole (Clethrionomys glareolus)

    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

• Related FAN Content :

  • 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

  • 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'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'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 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