Abstract

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  • Fluoride-induced oxidative stress and apoptosis are involved in the reducing of oocytes development potential in mice.

    The present study was conducted to investigate the mechanisms of excessive-fluoride-induced reduction of oocyte development potential in mice. The development morphology of oocyte and the changes of pathomorphology in ovary were observed. The protein expression levels of apoptosis factors, including Bax, Bcl-2, casepase-3, casepase-9 and cytochrome c, and the mRNA

  • Fluoride Impairs Ovary Development by Affecting Oogenesis and Inducing Oxidative Stress and Apoptosis in Female Zebrafish (Danio Rerio).

    Highlights Fluoride exposure decreased FSH, LH and VTG levels in ovary of zebrafish. Fluoride exposure altered the transcriptional profiles of oogenesis-related genes. Fluoride exposure increased ROS production in ovary of zebrafish. Fluoride exposure induces oxidative stress in ovary of zebrafish. Fluoride exposure induces apoptosis through both extrinsic and intrinsic

  • 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

  • Sodium fluoride adversely affects ovarian development and reproduction in Drosophila melanogaster.

    The study demonstrates the effects of chronic sub-lethal exposure of sodium fluoride (NaF) on reproductive structure and function of female Drosophila melanogaster. As a part of treatment, flies were maintained in food supplemented with sub-lethal concentrations of NaF (10-100 ?g/mL). Fecundity, ovarian morphology, presence and profusion of viable cells from ovary

  • Sodium fluoride induces apoptosis through reactive oxygen species-mediated endoplasmic reticulum stress pathway in Sertoli cells

    Excessive fluoride exposure is known to contribute to reproductive system dysfunction, ultimately leading to pathological damage and apoptosis in cells. Although both oxidative and endoplasmic reticulum (ER) stresses have been implicated in fluorosis, the signaling pathways and their roles in sodium fluoride (NaF)-induced apoptosis of Sertoli cells have been sparsely

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  • 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 - Human Studies

    Consistent with in vitro and animal research, studies of human populations have reported associations between fluoride exposure and damage to the male reproductive system. Most notably, a scientist at the Food & Drug Administration reported in 1994 that populations in the United States with more than 3 ppm fluoride in their water had lower "total fertility rates" than populations with lower fluoride levels.

  • Fluoride's Effect on Male Reproductive System: Animal Studies

    Over 60 studies on animals (including rats, mice, roosters, and rabbits) have found that fluoride adversely impacts the male reproductive system. These studies have repeatedly found the following effects: (1) decreases in testosterone levels; (2) reduced sperm motility; (3) altered sperm morphology; (4) reduced sperm quantity; (5) increased oxidative stress; (6) and reduced capacity to breed.

  • 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 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