Abstract

Chronic fluoride (Fl) toxicity is a serious public health problem globally where drinking water contains more than 1 ppm of Fl. Sodium fluoride (NaF) produced male reproductive system toxicity. The aim of the present study was to evaluate the amelioration of Fl toxicity-induced fertility impairment by vitamin E and calcium during the withdrawal period. The study was carried out on 70 adult male albino rats divided into five main groups: group I control; subdivided into group Ia (maintained on standard diet and water ad libitum for 60 days) and group Ib (maintained on standard diet and water ad libitum for 120 days), group II was administered NaF and subdivided into group IIa (administered NaF for 60 day and sacrificed) and group IIb (administered NaF for 60 day then maintained on standard diet and water ad libitum for a further 60 days), and treated groups III, IV, and V were administered NaF. Rats were maintained during withdrawal from NaF, on vitamin E (10 mg kg?1 day?1 for 60 days), calcium (50 mg kg?1 day?1 orally for 60 days), and both vitamin E and calcium, respectively. The duration of NaF administration was 60 days at a dose 20 mg kg?1 day?1 for all treated groups. The following parameters were determined: body and organ weights, sperm motility, sperm morphology, sperm viability, fertility test, and hormone assays: testosterone, in vitro testosterone production, luteinizing hormone, and follicular stimulating hormone. The combined administration of vitamin E and calcium during withdrawal from NaF showed significant improvement from chronic FL-induced toxicity on male reproductive organs.

• Related Studies :

  • Amelioration of fluoride toxicity in rats through vitamins (C, D) and calcium

    The healthy, adult male rats (Rattus norvegicus) were treated with fluoride water (F.W.+5.8 ppm), F.W.+ ascorbic acid and F.W. + vitamins (C, D) and Ca+2 for 60 days. Fluoride water ingestion to rats for 60 days resulted in significant reduction of seminal vesicle weight, sperm motility and sperm density of

  • 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

  • Reversal of fluoride-induced alteration in cauda epididymal spermatozoa and fertility impairment in male mice

    The effects of sodium fluoride (NaF) ingestion (10 mg NaF/kg body weight) and the possible therapeutic effects of ascorbic acid (AA, 15 mg/animal/day) and/or calcium phosphate (Ca, 25 mg/animal/day) on the reproductive functions and fertility of male mice were investigated. NaF-ingestion brought about a significant decline in sperm acrosomal acrosin

  • 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

  • Amelioration of fluoride toxicity in some accessory reproductive glands and spermatozoa of rat

    Sodium fluoride (NaF) at a dose of 10 mg/kg body weight was administered orally to male rats (Rettus norvegicus) daily for 30 and 50 days to evaluate the effect of the physiology of some sex accessory glands and sperm functions. The effects of withdrawal upon cessation of NaF ingestion, and

• Related FAN Content :

  • 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 & 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

  • Kidney Patients Are at Increased Risk of Fluoride Poisoning

    It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients

  • 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: 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.