Abstract
The toxicity of sodium fluoride (NaF) to female fertility is currently recognized; however, the mechanisms are unclear. Previously, we reported a reduction in successful pregnancy rates, ovarian atrophy and dysfunction following exposure to NaF. The purpose of this study was to elucidate the underlying molecular mechanisms. Female Sprague-Dawley rats (10 rats/group) received 100 or 200mg/L NaF in their drinking water for 6 months or were assigned to an untreated control group. Apoptotic indices and oxidative stress indicators in blood and ovarian tissue were analyzed following sacrifice. The results confirmed the NaF-induced ovarian apoptosis, with concomitant activation of oxidative stress. Further investigations in ovarian granular cells showed that exposure to NaF activated extracellular regulated protein kinase (ERK) and c-Jun NH2 kinase (JNK), disrupting the ERK and JNK signaling pathways, while p38 and PI3K remained unchanged. These data demonstrated that oxidative stress may play a key role in NaF-induced ovarian dysfunction by activating the apoptotic ERK and JNK signaling pathways.
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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
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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
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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
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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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Toxic effects of fluoride on reproductive ability in male rats: sperm motility, oxidative stress, cell cycle, and testicular apoptosis.
To investigate the effects of sodium fluoride (NaF) on sperm motility, oxidative stress, and apoptosis in the testes, male Wistar rats were exposed to 1.0, 2.0, and 3.0 mg NaF/kg bw/day by intragastric gavage for 90 days. Sperm motility was significantly inhibited, especially at the lower F intake level. Significant
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Fluoride content in tea and its relationship with tea quality.
J Agric Food Chem. 2004 Jul 14;52(14):4472-6. Fluoride content in tea and its relationship with tea quality. Lu Y, Guo WF, Yang XQ. Department of Tea Science, Zhejiang University, 268 Kaixuan Road, Hangzhou 310027, People's Republic of China. Abstract: The tea plant is known as a fluorine accumulator. Fluoride (F) content in fresh leaves collected
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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.
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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,
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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.
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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.
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