Chronic Exposure to Fluoride Affects GSH Level and NOX4 Expression in Rat Model of This Element of Neurotoxicity.
Animals
Brain
/ enzymology
Disease Models, Animal
Female
Gene Expression Regulation, Enzymologic
/ drug effects
Glutathione
/ metabolism
NADPH Oxidase 4
/ biosynthesis
Neurotoxicity Syndromes
/ enzymology
Oxidative Stress
/ drug effects
Pregnancy
Prenatal Exposure Delayed Effects
/ enzymology
Rats
Rats, Wistar
Reactive Oxygen Species
/ metabolism
Sodium Fluoride
/ toxicity
Up-Regulation
/ drug effects
GSH
NOX4
brain
fluoride
neurotoxicity
oxidative stress
Journal
Biomolecules
ISSN: 2218-273X
Titre abrégé: Biomolecules
Pays: Switzerland
ID NLM: 101596414
Informations de publication
Date de publication:
09 03 2020
09 03 2020
Historique:
received:
10
01
2020
revised:
25
02
2020
accepted:
26
02
2020
entrez:
19
3
2020
pubmed:
19
3
2020
medline:
19
3
2021
Statut:
epublish
Résumé
Exposure of neural cells to harmful and toxic factors promotes oxidative stress, resulting in disorders of metabolism, cell differentiation, and maturation. The study examined the brains of rats pre- and postnatally exposed to sodium fluoride (NaF 50 mg/L) and activity of NADPH oxidase 4 (NOX4), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), concentration of glutathione (GSH), and total antioxidant capacity (TAC) in the cerebellum, prefrontal cortex, hippocampus, and striatum were measured. Additionally, NOX4 expression was determined by qRT-PCR. Rats exposed to fluorides (F-) showed an increase in NOX4 activity in the cerebellum and hippocampus, a decrease in its activity in the prefrontal cortex and hippocampus, and upregulation of NOX4 expression in hippocampus and its downregulation in other brain structures. Analysis also showed significant changes in the activity of all antioxidant enzymes and a decrease in TAC in brain structures. NOX4 induction and decreased antioxidant activity in central nervous system (CNS) cells may be central mechanisms of fluoride neurotoxicity. NOX4 contributes to blood-brain barrier damage, microglial activation, and neuronal loss, leading to impairment of brain function. Fluoride-induced oxidative stress involves increased reactive oxygen speciaes (ROS) production, which in turn increases the expression of genes encoding pro-inflammatory cytokines.
Identifiants
pubmed: 32182821
pii: biom10030422
doi: 10.3390/biom10030422
pmc: PMC7175316
pii:
doi:
Substances chimiques
Reactive Oxygen Species
0
Sodium Fluoride
8ZYQ1474W7
NADPH Oxidase 4
EC 1.6.3.-
Nox4 protein, rat
EC 1.6.3.-
Glutathione
GAN16C9B8O
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Déclaration de conflit d'intérêts
The authors declare they have no actual or potential competing financial interests.
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