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 :

  • Alterations in the memory of rat offspring exposed to low levels of fluoride during gestation and lactation: Involvement of the a7 nicotinic receptor and oxidative stress.

    Daily exposure to fluoride (F) depends mainly on the intake of this element with drinking water. When administered during gestation and lactation, F has been associated with cognitive deficits in the offspring. However, the mechanisms underlying the neurotoxicity of F remain obscure. In the current study, we investigated the effects

  • Sirt3-mediated mitochondrial dysfunction is involved in fluoride-induced cognitive deficits.

    Highlights Fluoride induces cognitive deficits in mice. Fluoride exposure results in neural/synaptic injury in the hippocampus of mice. Mitochondrial dysfunction contributes to neural/synaptic alternations. Inhibition of Sirt3 is involved in the fluoride-evoked mitochondrial abnormalities. Abstract Excessive fluoride is capable of inducing cognitive deficits, but the mechanisms remain elusive. This study aimed

  • The analog of Ginkgo biloba extract 761 is a protective factor of cognitive impairment induced by chronic fluorosis.

    Ginkgo biloba extract EGb761 is widely used to treat patients with learning and memory impairment in Alzheimer's disease and Parkinson's disease in China. However, it is not yet clear whether the analog of EGb761 (EGb) has a protective effect on the learning and memory damage induced by chronic fluorosis. In

  • Changed expressions of N-methyl-D-aspartate receptors in the brains of rats and primary neurons exposed to high level of fluoride

    Expressions of N-methyl-d-aspartic acid receptors (NMDARs) in the brains of rats and primary neurons exposed to high fluoride were investigated. Sprague-Dawley rats were divided randomly into a fluorosis group (50 ppm fluoride in the drinking water for 6 months) and controls (<0.5ppm fluoride) and the offspring from these rats sacrificed

  • Fluoride-induced neuron apoptosis and expressions of inflammatory factors by activating microglia in rat brain

    Excessive exposure to fluoride results in structural and functional damages to the central nervous system (CNS), and neurotoxicity of fluoride may be associated with neurodegenerative changes. Chronic microglial activation appears to cause neuronal damage through producing proinflammatory cytokines and is involved in many neurodegenerative disorders. It is not known about

• 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: 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 & IQ: 76 Studies

    • As of July 18, 2022, a total of 85 human studies have investigated the relationship between fluoride and human intelligence. • Of these investigations, 76 studies have reported that elevated fluoride exposure is associated with reduced IQ in humans. • The studies which reported an association of reduced IQ with exposure

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

    The NRC's analysis on fluoride and the brain.

  • 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.