Abstract

A study was made of the effect of fluoride on oxidative stress in rats during their early stages in life. Wistar albino rats were exposed to 30 ppm and 100 ppm fluoride (from sodium fluoride) in drinking water during the last one week of intrauterine life and then up to ten weeks after birth. Oxidative stress was evaluated by the assays of malondialdehyde and antioxidants in brain homogenates. Malondialdehyde (MDA), the marker of extent of lipid peroxidation, was elevated in the brain of rats treated with 100 ppm fluoride but was without change in rats treated with 30 ppm fluoride. Levels of total glutathione, reduced glutathione (GSH), and ascorbic acid (vitamin C) were elevated in 30 ppm fluoride-treated rats, while these levels decreased in 100 ppm fluoride-treated rats. The activity of glutathione peroxidase (GSH-Px) was elevated significantly in both 30 ppm and 100 ppm fluoride-treated rats. Glutathione S-transferase (GST) activitiy in the brain increased with 30 ppm and 100 ppm fluoride, and greater elevation occurred at 30 ppm. These results suggest that fluoride enhances oxidative stress in the brain, thereby disturbing the antioxidant defense of rats. Increased oxidative stress could be one of the mediating factors in the pathogenesis of fluoride toxicity in the brain.

• Related Studies :

  • [Influence of free radical inducer on the level of oxidative stress in brain of rats with fluorosis].

    OBJECTIVE:  To study changes in content of lipid peroxide and composition of fatty acids in the brain of rats affiliated with chronic fluorosis after treatment with free radical inducer (ferric ion). METHODS:  Thirty-six Wistar rats were divided into three groups, fed with similar fodder and varied concentrations of fluoride in drinking

  • Effects of sodium fluoride on lipid peroxidation and PARP, XBP-1 expression in PC12 cell

    This study aims to clarify the molecular mechanism of fluorine exposure that leads to nerve injury. PC12 cells were treated with fluorine at different concentrations (0.5, 1.0, 1.5, and 2.0 mM). Cytoactivity was detected at different time points (2, 4, 6, 8, 12, 24, and 48 h). After 2 h, DCF was used

  • Apoptotic and Degenerative Changes in the Enteric Nervous System Following Exposure to Fluoride During Pre- And Post-natal Periods.

    Children born in fluorosis endemic areas usually suffer from gastrointestinal complications and are unable to attain normal growth as per their age group. The enteric nervous system (ENS) controls gut movement and functions. It is highly vulnerable to any ingested toxins. Based on observations, it was hypothesized that fluoride exposure

  • Activation of the AGE/RAGE system in the brains of rats and in SH-SY5Y cells exposed to high level of fluoride might connect to oxidative stress

    To explore the mechanisms by which chronic fluorosis damages the brain, we determined the levels of the advanced glycation end-products (AGEs), the receptor for AGE (RAGE), NADPH oxidase-2 (NOX2), reactive oxygen species (ROS) and malondialdehyde (MDA) in the brains of rats /and or SH-SY5Y cells exposed to different levels of sodium fluoride

  • Effects of fluoride accumulation on some enzymes of brain and gastrocnemius muscle of mice

    This study reports accumulation of fluoride and altered activities of some enzymes involved in free-radical metabolism and membrane function in whole brain and gastrocnemius muscle of female mice treated with NaF (20mg/kg/body weight) for 14 days. The body weight and somatic index were decreased, whereas fluoride levels were significantly increased

• Related FAN Content :

  • NRC (2006): Fluoride's Neurotoxicity and Neurobehavioral Effects

    The NRC's analysis on fluoride and the brain.

  • Fluoride's Effect on Fetal Brain

    The human placenta does not prevent the passage of fluoride from a pregnant mother's bloodstream to the fetus. As a result, a fetus can be harmed by fluoride ingested pregnancy. Based on research from China, the fetal brain is one of the organs susceptible to fluoride poisoning. As highlighted by the excerpts

  • 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

  • Fluoride & IQ: The 65 Studies

    As of May 2020, a total of 73 studies have investigated the relationship between fluoride and human intelligence. Of these investigations, 65 studies have found that elevated fluoride exposure is associated with reduced IQ in humans, while over 60 animal studies have found that fluoride exposure impairs the learning and/or

  • 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,