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  • Chronic fluoride exposure alters antioxidant enzymes in rat brain and intestine

    Background: Low Fluoride use has been advocated as a therapeutic agent for delaying tooth decay however, high fluoride exposure has been associated with behavioral changes, low IQ, and altered brain functions and development. Although Fluoride generally does not generate free radicals but is still implicated in free radical associated damage

  • [Influence of combined iodine and fluoride on phospholipid and fatty acid composition in brain cells of rats].

    OBJECTIVE:  Investigating the influence of combined iodine and fluoride on phospholipid and fatty acid composition in brain cells of rats. METHODS:  Five groups of rats were provided with deionized drinking water containing 0 and 150 mg/L NaF, and containing both 150 mg/L NaF and 0.003, 0.03 or 3 mg/L KI respectively

  • Protective effect of ascorbic acid and Ginkgo biloba against learning and memory deficits caused by fluoride.

    Fluoride is present in the ground water, World Health Organization permitted level of fluoride in the ground water is 0.5 ppm. Tooth pastes, mouth washes, tea and sea fish are the sources of fluoride. Exposure to these multiple sources results in several adverse effects in addition to the fluorosis. The

  • Health effects of selected chemicals. 3. Cryolite (sodium aluminium fluoride)

    Cryolite occurs in the nature as monoclinic crystals or in synthetic form as an amorphous powder. The natural form may be coloured reddish or brown or even black. Cryolite has a melting point >1 000 degrees C and its main use is in the production of aluminum where it forms

  • ERK1/2-mediated disruption of BDNF–TrkB signaling causes synaptic impairment contributing to fluoride–induced developmental neurotoxicity

    Highlights Rats were long–term chronic exposed to environmentally relevant doses of fluoride. Fluoride exposure results in synaptic alterations both in vivo and in vitro. Fluoride–induced cognitive failures correlates with synaptic deficits. BDNF–TrkB axis disruption contributes to fluoride–elicited impaired synaptogenesis. ERK1/2 plays a vital role in fluoride–induced BDNF–TrkB signaling disruption. Excessive

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