Abstract
Background: Curcumin (Cur), an active ingredient of turmeric is known to have multiple activities, including an antioxidant property and has been suggested to be useful in treatment of several neurological diseases.
Objective: To investigate the neuroprotective effects of Cur to mitigate the effect of the Fluoride (F) induced neurotoxicity in mice brain using the histological and the biochemical parameters.
Materials and Methods: Exposure of mice (30 days old male) to F (120 ppm) daily for 30 days.
Result and Discussion: Treatment with the F causes an increase in lipid peroxidation (LPO) and also increase in the neurodegenerative cells in the hippocampal sub-regions. Interestingly, co-treatment with Cur (30 mg/kg BW) with F (120 ppm) for 30 days results in significant decreases in LPO with a concomitant decrease in neurodegeneration as compared with those treated with F alone.
Conclusion: Our study reveals that Cur is useful in ameliorating degenerative effects of F in mice brain.
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Combined impact of exercise and temperature in learning and memory performance of fluoride toxicated rats.
In previous studies, we investigated a link between high fluoride exposure and functional IQ deficits in rats. This study is an extension conducted to explore the combined influence of physical exercise and temperature stress on the learning ability and memory in rats and to assess whether any positive modulation could
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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
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Suppression of mitochondrial oxidative phosphorylation and TCA enzymes in discrete brain regions of mice exposed to high fluoride: amelioration by Panax ginseng (Ginseng) and Lagerstroemia speciosa (Banaba) extracts
Chronic fluoride intoxication results in pathophysiological complications pertaining to soft tissues, called non-skeletal fluorosis. This study examined whether fluoride-induced alterations in selected parameters that are indicative of mitochondrial dysfunction accompany the toxic effects of fluoride in discrete brain regions in vivo and also explored the possibility of treatment with Ginseng
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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
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Effects of fluoride on the expression of NCAM, oxidative stress, and apoptosis in primary cultured hippocampal neurons.
The mechanisms underlying the neurotoxicity of endemic fluorosis still remain unknown. To investigate the expression level of neural cell adhesion molecules (NCAM), oxidative stress, and apoptosis induced by fluoride, the primary rat hippocampal neurons were incubated with 20, 40, and 80 mg/l sodium fluoride for 24 h in vitro. The
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Fluoride's Direct Effects on Brain: Animal Studies
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