Abstract

Effects of exposure of Swiss albino adult male mice to 17.6 mg NaF/L in their drinking water for up to 30 days on the NADPH diaphorase (NADPH-d) positive neurons in the forebrain were studied. Histochemical study by the method developed by Hope and Vincent for the distribution of NADPH-d positive neuron cell bodies was conducted in the cerebral cortex, hippocampus, amygdala, caudate putamen, and selected nuclei of the hypothalamus. Counting neuronal cell bodies, their dendritic intersections, and varicosities in the brain of the F-exposed mice showed significant increase in the neuron cell bodies. In the cerebral cortex, amygdala, and caudate putamen, the increase in the number of NADPH-d positive neurons and their dendritic intersections was highly significant (p<0.05), but no significant difference was seen in the dendritic branching. A significant increase in the number of varicosities was also observed in the brain of the F-treated mice. These results indicate that excessive F intake caused morphological changes in NADPH-d/NOS (nitric oxide synthase) positive neurons in the brain, thus increasing nitric oxide (NO) synthesis, which is implicated in F-induced neuron cell death. A possible mechanism of F neurotoxicity is thereby suggested.

• Related Studies :

  • Systematic impacts of fluoride exposure on the metabolomics of rats.

    Highlights The risk of chronic endemic fluorosis exists in many countries and regions. Comprehensive metabolomic analysis was used to study the effects of fluoride. Multivariate statistics were used to detect metabolite profile changes. Fluoride exposure caused amino acid, fatty acid, and energy metabolism disorders. Fluoride exposure caused oxidative stress,

  • Evaluation of fluoride-induced oxidative stress in rat brain: a multigeneration study.

    Multigenerational evaluation was made in rats on exposure to high fluoride (100 and 200 ppm) to assess neurotoxic potential of fluoride in discrete areas of the brain in terms of lipid peroxidation and the activity of antioxidant enzyme system. The rats were given fluoride through drinking water (100 and 200 ppm) and

  • AMPK/p38/Nrf2 activation as a protective feedback to restrain oxidative stress and inflammation in microglia stimulated with sodium fluoride.

    Highlights NaF-stimulated redox imbalance and inflammation. NaF activated the Nrf2 signaling in BV-2 cells and primary cultured microglia. Nrf2 activation exerts a neuroprotective effect on NaF-stimulated redox imbalance and inflammation. ROS-AMPK-p38 signaling is the upstream signaling pathway involved in NaF-induced Nrf2 activation. Dysregulated activation of inflammation plays an important role in the

  • Quercetin treatment against NaF induced oxidative stress related neuronal and learning changes in developing rats

    Previous behavioural studies shows that excessive exposure of fluoride caused diminished intelligent quotient in children compared to the normal children (Wang et al., 2004) and sodium fluoride intoxicated rat exerted loss of memory and learning disability (Yaning et al., 2005). In the present study postnatal rats aged day 21 and

  • Neurobehavioral and neurochemical effects in rats offspring co-exposed to arsenic and fluoride during development.

    Highlights Arsenic/Fluoride co-exposure during development causes neurobehavioral alterations in offspring. iAs/F causes delayed development of sensorimotor reflexes and produces less nociceptive response. iAs/F co-exposure increase locomotor activity. Antioxidant enzymes and neurotransmitter level are altered in the striatum area. Arsenic (iAs) and fluoride (F) are ubiquitous in the environment. All over

• Related FAN Content :

  • 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 content in tea and its relationship with tea quality.

    J Agric Food Chem. 2004 Jul 14;52(14):4472-6. Fluoride content in tea and its relationship with tea quality. Lu Y, Guo WF, Yang XQ. Department of Tea Science, Zhejiang University, 268 Kaixuan Road, Hangzhou 310027, People's Republic of China. Abstract: The tea plant is known as a fluorine accumulator. Fluoride (F) content in fresh leaves collected

  • Fluoride: Developmental Neurotoxicity.

    Developmental Neurotoxicity There has been a tremendous amount of research done on the association of exposure to fluoride with developmental neurotoxicity. There are over 60 studies reporting reduced IQ in children and several on the impaired learning/memory in animals. And there are studies which link fluoride to Attention Deficit Hyperactivity Disorder. Teaching

  • 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.