Abstract
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 study aimed to investigate the possible neuroprotective role of tert-butylhydroquinone (tBHQ), a general Nrf2 activator, on sodium fluoride (NaF)-induced oxidation damage and apoptosis in neuron-like rat pheochromocytoma (PC12) cells. Pretreatment with tBHQ protected PC12 cells against NaF-induced cytotoxicity as measured by MTT assay and apoptosis detection, simultaneously, inhibited NaF-induced overproduction of intracellular ROS and reduction of total glutathione content. Furthermore, NaF or tBHQ induced the stabilization of Nrf2, and enhanced expression of heme oxygenase-1 (HO-1) and ?-glutamylcysteine synthetase (?-GCS) as a consequence of Nrf2 inducing. These findings indicated that tBHQ pretreatment conferred protective effect on PC12 cells against NaF-induced apoptotic cell death and oxidation-redox imbalance through stabilization of Nrf2 and elevation of downstream HO-1 and ?-GCS expressions.
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Protective role of maize purple plant pigment against oxidative stress in fluorosis rat brain.
Excerpts 1 Introduction Given the widespread presence of fluorine in the natural environment, individuals are exposed to fluoride via food intake, inhalation, and dermal contact. Drinking water represents the largest exposure source. In particular, in highly fluoridated regions and in some developed areas that fluoridate the public water supply to reduce dental
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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
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Neuroprotective effect of ascorbic acid and ginkgo biloba against fluoride caused neurotoxicity
Excessive consumption of fluoride through drinking water or other sources lead to skeletal and dental fluorosis. According to the world health organization 23 nations are facing the problem of fluorosis. In the recent past researchers describe the non-skeletal fluorosis where soft tissues and major organs are the victims of fluoride
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Apoptotic and Degenerative Changes in the Enteric Nervous System Following Exposure to Fluoride During Pre- And Post-natal Periods.
Children born in fluorosis endemic areas usually suffer from gastrointestinal complications and are unable to attain normal growth as per their age group. The enteric nervous system (ENS) controls gut movement and functions. It is highly vulnerable to any ingested toxins. Based on observations, it was hypothesized that fluoride exposure
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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
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Developmental Neurotoxicity There has been a tremendous amount of research done on the association of exposure to fluoride with developmental neurotoxicity. There are 78 studies reporting reduced IQ (75 studies with children and 3 studies with adults) and several on the impaired learning/memory in animals. And there are studies which link
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