Abstract

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 multiple hormone systems that impact male reproduction. The changes in spermatozoa result from oxidative damage, zinc deficiency, and disturbed signal transduction. There is evidence that F interferes with spermatogenesis by depressing levels of epidermal growth factor (EGF) and epidermal growth factor receptor (EGFR), modifying G-protein signaling, diminishing levels of testosterone and its androgen receptor (AR), and disturbing levels of estradiol. Furthermore, F is also known to interfere with thyroid hormone metabolism, which directly and indirectly impacts not only spermatogenesis but also other reproductive functions. Although F appears to exert its toxic effects in the male reproductive system through these pathways, the molecular details are still poorly understood. The growing evidence that F overexposure leads to male reproductive toxicity through multiple pathways indicates that an assessment of chronic F exposures in human and animal populations is urgently required.

• 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

  • NADPH oxidase participates in the oxidative damage caused by fluoride in rat spermatozoa. Protective role of a-tocopherol

    Fluorosis, caused by drinking water contaminated with inorganic fluoride, is a public health problem in many areas around the world. The aim of this study was to evaluate oxidative stress in spermatozoa caused by fluoride and NADPH oxidase in relationship to fluoride. Four experimental groups of male Wistar rats were

  • Toxic effects of sodium fluoride on reproductive function in male mice

    To investigate the effects and possible mechanisms of the action of fluoride on testis cell cycle and cell apoptosis in male mice, sexually mature male Kunming mice were exposed to 50, 100, 200, and 300 mg NaF/L in their drinking water for 8 weeks. At the end of the exposure

  • Selenium may suppress peripheral blood mononuclear cell apoptosis by modulating HSP70 and regulate levels of SIRT1 through reproductive hormone secretion and oxidant stress in women suffering fluorosis.

    Excessive taking fluoride (F) causes severe damage to reproductive system through stimulation of apoptosis and oxidant stress. Selenium (Se) may promote anti-oxidant enzymes and invert cell apoptosis. The aim of this study was to investigate the effect of Se on peripheral blood mononuclear cell (PBMC) apoptosis and oxidant stress in

  • Effects of sodium fluoride and sulfur dioxide on oxidative stress and antioxidant defenses in rat testes

    To assess effects of sodium fluoride and sulfur dioxide on oxidative stress and antioxidant defenses in the testes, 96 sexually mature male Wistar rats were divided randomly into four groups of twenty-four rats each. One group of rats was left untreated as controls, and the other three groups were administered,

• Related FAN Content :

  • 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

  • Is fluoride-induced hyperthyroidism a cause of psychosis among East African immigrants to Scandinavia?

    When people with a compensated fluoride-induced hypothyroidism move to a low-fluoride area, the fluoride-induced inhibition of the production of thyroid hormones ceases. In Scandinavia, the dietary intake of iodine is usually quite high due to iodized table salt and easy access to marine fish. Under these conditions, the elevated capacity for production of thyroid hormones may result in hyperthyroidism.

  • Mikhailets (1996): Functional state of thyroid under extended exposure to fluorides

    Abnormalities in the thyroid function characterized by a decreased iodine absorption function of the thyroid, a low level T3 syndrome, and a slight increase of the TSH level are observed in cases of chronic fluorine intoxication in the industrial workers.

  • Fluoride, Water Hardness, and Endemic Goitre

    Variations in goitre prevalence were found to correlate closely with the fluoride content (p=0-74; P<0-01) and with the hardness (p=0.77; P<0-01) of the water in each village. The effects of fluoride and water hardness seem to be independent.