Abstract

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  • Cell cycle arrest and gene expression profiling of testis in mice exposed to fluoride

    Exposure to fluoride results in low reproductive capacity; however, the mechanism underlying the impact of fluoride on male [re]productive system still remains obscure. To assess the potential toxicity in testis of mice administrated with fluoride, global genome microarray and real-time PCR were performed to detect and identify the altered transcriptions.

  • 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

  • Interleukin 17A deficiency alleviates fluoride-induced testicular injury by inhibiting the immune response and apoptosis.

    Highlights Exposure to high-levels of fluoride causes reproductive toxicity in humans. Increased testes toxicity and inflammation were seen in a mouse model of fluorosis. The NaF-mediated testes toxicity and inflammation were absent in IL-17A -/- mice. In Leydig cells IL-17A and/or NaF increased apoptosis and decreased testosterone. Il-17A appears

  • Effects of Fluoride on Surface Structure of Primary Culture Leydig Cells in Mouse.

    Fluoride (F) is known to induce reproduction toxicity, and the elucidation of its underlying mechanisms is an ongoing research. These findings aim to provide deeper insights into roles of soduim fluoride (NaF) in testis damage, which could contribute to a better understanding of fluoride-induced male reproductive toxicity. The Leydig cells

  • Fluoride-Induced Sperm Damage and HuR-Mediated Excessive Apoptosis and Autophagy in Spermatocytes.

    It is critical to determine the mechanism underlying fluoride (F)-induced damage of the testes to develop appropriate strategies for monitoring and intervention. In the present study, exposure to 50 mg/L sodium fluoride (NaF) for 90 days damaged the normal structure of the testes and quality of the sperm, particularly the spermatocytes, and

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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.

  • 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