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

• Published in: Archives of toxicology 2006-10, Vol.80 (10), p.671-679
• Main Authors: ÖZTÜRK, Oktay Hasan, KÜCÜKATAY, Vural, YÖNDEN, Zafer, AGAR, Aysel, BAGCI, Hüseyin, DELIBAS, Namik
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Cognition - drug effects; Down-Regulation; Hippocampus - drug effects; Hippocampus - metabolism; Liver - drug effects; Liver - enzymology; Male; Medical sciences; Protein Subunits - drug effects; Rats; Rats, Wistar; Receptors, N-Methyl-D-Aspartate - drug effects; Receptors, N-Methyl-D-Aspartate - metabolism; Rodents; Sulfite Oxidase - deficiency; Sulfites - toxicity; Time Factors; Toxicology
• ISSN: 0340-5761; 1432-0738
• DOI: 10.1007/s00204-006-0125-x

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 endogenous 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.