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-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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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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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
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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
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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'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
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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 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 & 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
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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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