Expressions of N-methyl-D-aspartate receptors NR2A and NR2B subunit proteins in normal and sulfite-oxidase deficient rat's hippocampus: effect of exogenous sulfite ingestion

Autor: Zafer Yonden, Vural Kucukatay, Aysel Agar, Namik Delibas, Oktay Hasan Ozturk, Huseyin Bagci
Rok vydání: 2006
Předmět:
Male
Time Factors
hippocampus
Health
Toxicology and Mutagenesis
Toxicology
Hippocampus
chemistry.chemical_compound
sulfite
Cognition
rat
Receptor
Heme
chemistry.chemical_classification
article
General Medicine
Amino acid
enzyme activity
Biochemistry
priority journal
Liver
Toxicity
Mammalia
enzyme deficiency
down regulation
medicine.medical_specialty
n methyl dextro aspartic acid receptor 2B
n methyl dextro aspartic acid receptor 2A
animal experiment
Down-Regulation
Receptors
N-Methyl-D-Aspartate
animal tissue
sulfite oxidase
Sulfite
male
Sulfite oxidase
Internal medicine
medicine
Animalia
Animals
Sulfites
controlled study
Rats
Wistar
protein expression
nonhuman
animal model
Sulfite Oxidase
protein subunit
Metabolism
Rats
Protein Subunits
Enzyme
Endocrinology
chemistry
nervous system
ingestion
Zdroj: Archives of toxicology. 80(10)
ISSN: 0340-5761
Popis: Sulfites whether ingested or produced through the sulfur-containing amino acids metabolism of the animal are very active molecules and can cause cellular toxicity. Sulfite oxidase (SOX), a heme- and molybdenum containing mitochondrial enzyme, prevents mammalian cells from adverse effects of sulfite toxicity by metabolizing sulfite to sulfate. The present study was aimed to investigate effect of sulfite on the N-methyl-d-aspartate (NMDA) receptor (NMDAR) NR2A and NR2B subunits in hippocampus of normal and SOX-deficient rats. Rats were divided into four groups; (1) control group, which was given rat chow and tap water ad libitum (C), (2) sulfite group, treated with sulfite (25 mg/kg) in drinking water and commercial rat chow ad libitum (S), (3) SOX-deficient group, maintained on high-W/Mo-deficient regimen to produce SOX deficiency (D), and (4) SOX-deficient + sulfite group (DS), prepared as those in the third group and were afterwards given sulfite (25 mg/kg) additionally. Whole treatment schedule were continued for 6 weeks. Sulfite treatment caused a decrease of NR2A and NR2B subunits of the NMDAR in hippocampus of rats in S and DS groups. Interestingly, similar decrement was observed in D group, probably due to increased endogen sulfite production. In summary, the results indicated that feeding sulfite to the rats may cause down-regulation of NMDARs by degrading NR2A and NR2B subunits of it, which may be considered as a neuro-compensatory mechanism. © Springer-Verlag 2006.
Databáze: OpenAIRE
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