Abstract

The mechanism of GSTO1, as a high-risk factor for neurological damage, in sodium fluoride (NaF)-induced learning and memory impairment remained still unclear. Hence, in this study, we used the siRNA-GSTO1 HT22 model to explore the effect of NaF and siRNA-GSTO1 on the viability, and proliferation rate of HT22cells, as well as the mRNA and protein expression levels of cyclic adenosine monophosphate (cAMP) response element binding protein (CREB), neural cell adhesion molecule (NCAM), stem cell factor (SCF) and brain-derived neurotrophic factor (BDNF). The results of MTT showed that 10^-3, 10^-4, and 10^-5 moL/L sodium fluoride (NaF) exposure could significantly promote the proliferation of HT22cells at 24 h, 36 h, and 48 h, respectively. In addition, our results showed that exposure to 10^-3, 10^-4, and 10^-5 moL/l NaF increased GSTO1 mRNA and protein expression, but decreased CREB and BDNF expression levels in a dose and time-dependent manner. The mRNA and protein expressions of GSTO1, CREB and BDNF were significantly decreased in the siRNA-GSTO1 and NaF + siRNA-GSTO1 group (P < 0.05). We have shown that various NaF doses affected the learning and memory ability by down-regulation the expressions of CREB, BDNF, NCAM and SCF. In summary, we concluded that GSTO1 plays a mediator role in NaF-induced neurological damage.

• Related Studies :

  • Attenuating effect of Vitamin E on the deficit of learning and memory of rats with chronic fluorosis: the mechanism may involve muscarinic acetylcholine receptors.

    The protective role of vitamin E (Vit E) against neurotoxicity induced by fluorosis was investigated by using Sprague-Dawley (SD) rats fed with 50 ppm fluoride in drinking water for 10 months. Spatial learning and memory of rats were measured by the Morris water maze test; the expressions of M1 and

  • The Effect of Chronic Fluorosis on Calcium Ions and CaMKIIa, and c-fos Expression in the Rat Hippocampus.

    This study investigated neurotoxicity of chronic fluorosis in the rat hippocampus. Newly weaning, male, Sprague-Dawley (SD) rats were administered 15, 30, and 60 mg/L sodium fluoride (NaF) solution (fluorine ion concentration 8.25, 16.50, and 33.00 mg/L, respectively), and tap water, for 18 months. The neurotoxicological mechanism was examined with a focus on intracellular

  • [Study of the mechanism of neurone apoptosis in rats from the chronic fluorosis].

    Objective: Study the mechanism of action chronic fluorosis in neurones. Methods: Terminal deoxyribo-nucleotide transferase-mediated dUTP-biotin nick end labeling (TUNEL) and flow cytometry (FCM) were used to observe changes of apoptosis in cerebral cells in chronic fluorosis in rats. Results: TUNEL results show non-random expression of DAB positive stain apoptosis cells which appear

  • Roles of mitochondrial fission inhibition in developmental fluoride neurotoxicity: mechanisms of action in vitro and associations with cognition in rats and children.

    Fluoride neurotoxicity is associated with mitochondrial disruption. Mitochondrial fission/fusion dynamics is crucial to maintain functional mitochondria, yet little is known about how fluoride perturbs this dynamics and whether such perturbation contributes to impaired neurodevelopment. Here in human neuroblastoma SH-SY5Y cells treated with sodium fluoride (NaF, 20, 40 and 60 mg/L), mitochondrial

  • Fisetin prevents fluoride- and dexamethasone-induced oxidative damage in osteoblast and hippocampal cells

    Fluoride intoxication and dexamethasone treatment produce deleterious effects in bone and brain. The aim of this study was to evaluate the effect of fluoride (F) and dexamethasone (Dex) co-exposure on oxidative stress and apoptosis in osteoblast-like MC3T3-E1 and hippocampal HT22 cell lines. Co-exposure to F and Dex resulted in a

• Related FAN Content :

  • Fluoride & IQ: 67 Studies

    As of May 2020, a total of 75 studies have investigated the relationship between fluoride and human intelligence. Of these investigations, 67 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

  • 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: 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

  • Fluoride Affects Learning & Memory in Animals

    An association between elevated fluoride exposure and reduced intelligence has now been observed in 65 IQ studies. Although a link between fluoride and intelligence might initially seem surprising or random, it is actually consistent with a large body of animal research. This animal research includes the following 45 studies (out

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

    The NRC's analysis on fluoride and the brain.