Abstract

The physiological toxicity of sodium fluoride on antioxidant system, organizational structure and apoptosis of brain tissue in Cyprinus carpio Linnaeus were studied. Results showed that along with the increasing concentration of sodium fluoride, the superoxide dismutase (SOD) and glutathione (GSH) activities increased firstly and then were inhibited after 30 days exposure. The SOD and GSH activities decreased after 60 and 90 days exposure. The content of lipid peroxides (MDA) increased during the whole test period. After 90 days exposure, histopathological changes of brain tissue were observed. It was found that thrombosis and structural changes in the cell layers were resulted from the exposure of sodium fluoride. The biological investigation results showed that there was a positive correlation between the cell apoptosis rate and the MDA levels (r = 0. 9968), but with dosage increasing, Bcl-2 protein concentration decreased, which was positive correlated with SOD and GSH activities (r =0. 9198 and 0. 9889, respectively).

• Related Studies :

  • Potential Role of Fluoride in the Etiopathogenesis of Alzheimer’s Disease.

    The etiopathogenesis of Alzheimer’s disease has not been fully explained. Now, the disease is widely attributed both to genetic and environmental factors. It is believed that only a small percentage of new AD cases result solely from genetic mutations, with most cases attributed to environmental factors or to the interaction

  • 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

  • Protective role of tert-butylhydroquinone against sodium fluoride-induced oxidative stress and apoptosis in PC12 cells.

    The neurotoxicity of fluoride is associated with oxidative stress due to imbalance between production and removal of reactive oxygen species (ROS). In contrast, induction of detoxifying and antioxidant genes through activation of NF-E2-related factor 2 (Nrf2) has been implicated in preventing oxidative stress and apoptosis in neurodegenerative diseases. The present

  • Rutin attenuates neurobehavioral deficits, oxidative stress, neuro-inflammation and apoptosis in fluoride treated rats.

    Highlights The influence of rutin on fluoride – induced neurotoxicity in rat was studied. Rutin reversed the fluoride – induced neurobehavioral deficits in rats. Rutin reversed the fluoride – induced inhibition of acetylcholinesterase activity in rat cerebrum and striatum. Rutin enhanced antioxidant status and inhibited neuro-inflammation and apoptosis in fluoride

  • Alterations of apoptosis and expressions of Bax and Bcl-2 in the cerebral cortices of rats with chronic fluorosis

    The aim of the study was to investigate the influence of chronic fluorosis on apoptosis and the expression of Bax and Bcl-2 in the cerebral cortices of rats in an attempt to elucidate molecular mechanisms. Sixty Sprague Dawley (SD) rats were divided randomly into three groups of 20 each: an

• 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's Direct Effects on Brain: Animal Studies

    The possibility that fluoride ingestion may impair intelligence and other indices of neurological function is supported by a vast body of animal research, including over 40 studies that have investigated fluoride's effects on brain quality in animals. As discussed by the National Research Council, the studies have consistently demonstrated that fluoride, at widely varying concentrations, is toxic to the brain.

  • 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

  • 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