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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

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dc.creator Yonden, Zafer
dc.creator Ozturk, Oktay Hasan
dc.creator Kucukatay, Vural
dc.creator Agar, Aysel
dc.creator Bagci, Huseyin
dc.creator Delibas, Namik
dc.date 2006-10-01T00:00:00Z
dc.date.accessioned 2021-12-03T12:04:12Z
dc.date.available 2021-12-03T12:04:12Z
dc.identifier e4f0b414-5cdc-4762-99fa-049f5bb8f84f
dc.identifier 10.1007/s00204-006-0125-x
dc.identifier https://avesis.sdu.edu.tr/publication/details/e4f0b414-5cdc-4762-99fa-049f5bb8f84f/oai
dc.identifier.uri http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/95479
dc.description 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.
dc.language eng
dc.rights info:eu-repo/semantics/closedAccess
dc.title 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
dc.type info:eu-repo/semantics/article


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