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.
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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
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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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Vitamin C and E supplementation can ameliorate NaF mediated testicular and spermatozoal DNA damages in adult Wistar rats.
Objective: Present study was designed to explore the efficacy of vitamin C and E (VC&VE) against fluoride mediated testicular, epididymal and spermatozoal anomalies. Materials and methods: Thirty two adult Wistar rats were divided into four groups. Group-I was control; Group-II received sodium fluoride (NaF) at 15 mg/kg/day
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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
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Synergistic effects of arsenic and fluoride on oxidative stress and apoptotic pathway in Leydig and Sertoli cells.
Highlights As and/or F reduced cell viability and proliferation in Leydig and Sertoli cells. As and/or F caused oxidative damage by increasing the ROS in TM3 and TM4 cells. As and/or F disrupted antioxidant enzymes activity in Leydig and Sertoli cells. As and/or F altered the expression levels of
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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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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 Is Not an Essential Nutrient
In the 1950s, dentists believed that fluoride was a “nutrient.” A nutrient is a vitamin or mineral that is necessary for good health. Dentists believed that fluoride ingestion during childhood was necessary for strong, healthy teeth. A “fluoride deficiency” was thus believed to cause cavities, just like a deficiency of calcium can
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Fluoride Exposure Aggravates the Impact of Iodine Deficiency
A consistent body of animal and human research shows that fluoride exposure worsens the impact of an iodine deficiency. Iodine is the basic building block of the T3 and T4 hormones and thus an adequate iodine intake is essential for the proper functioning of the thyroid gland. When iodine intake is inadequate during infancy and
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Fluoride Aggravates Thyroid Damage Caused by Excess Iodine Intake
Chinese researchers have found that the combination of excess fluoride with excess iodine caused greater reductions in IQ, or greater increases in goitre than either scenario by itself.
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