Please use this identifier to cite or link to this item:
https://hdl.handle.net/11499/6316
Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ozturk, O.H. | - |
dc.contributor.author | Oktar, S. | - |
dc.contributor.author | Aydin, M. | - |
dc.contributor.author | Küçükatay, Vural | - |
dc.date.accessioned | 2019-08-16T12:05:55Z | |
dc.date.available | 2019-08-16T12:05:55Z | |
dc.date.issued | 2010 | - |
dc.identifier.issn | 1138-7548 | - |
dc.identifier.uri | https://hdl.handle.net/11499/6316 | - |
dc.identifier.uri | https://doi.org/10.1007/s13105-010-0025-7 | - |
dc.description.abstract | Sulfite and related chemical such as sulfite salts and sulfur dioxide has been used as a preservative in food and drugs. This molecule has also been generated from the catabolism of sulfur-containing amino acids. Sulfite is a very reactive and potentially toxic molecule and has to be detoxified by the enzyme sulfite oxidase (SOX). The aim of this study was to investigate the effects of ingested sulfite on erythrocyte antioxidant status by measuring glucose-6-phosphate dehydrogenase (G-6-PD), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities and oxidant status by measuring thiobarbituric acid reactive substances (TBARS) in normal and SOX-deficient rats. Rats were assigned to four groups (n=10 rats/group) as follows; control (C), sulfite (CS), deficient (D), and deficient+sulfite (DS). SOX deficiency was established by feeding rats a low molybdenum diet and adding to their drinking water 200 ppm tungsten (W). Sulfite (25 mg/kg) was administered to the animals via their drinking water. At the end of 6 weeks, Erythrocyte G-6-PD, SOD, and GPx but not CAT activities were found to be significantly increased with and without sulfite treatment in SOX-deficient groups. Sulfite treatment alone was also significantly increased erythrocytes' SOD activity in CS group compared to control. TBARS levels were found to be significantly increased in CS and DS groups and decreased in D group. When SOX-deficient rats treated with sulfite, TBARS level was still higher than other groups. In conclusion, these results suggested that erythrocyte antioxidant capacity, a defense mechanism against the oxidative challenge, increased by endogenous and exogenous sulfite due to its oxidant nature. This increase was also observed in CS and DS groups but it was insufficient to prevent lipid peroxidation. © 2010 University of Navarra. | en_US |
dc.language.iso | en | en_US |
dc.relation.ispartof | Journal of Physiology and Biochemistry | en_US |
dc.rights | info:eu-repo/semantics/closedAccess | en_US |
dc.subject | Antioxidants | en_US |
dc.subject | Erythrocyte | en_US |
dc.subject | Lipid peroxidation | en_US |
dc.subject | Rat | en_US |
dc.subject | Sulfite | en_US |
dc.subject | catalase | en_US |
dc.subject | drinking water | en_US |
dc.subject | glucose 6 phosphate dehydrogenase | en_US |
dc.subject | glutathione peroxidase | en_US |
dc.subject | molybdenum | en_US |
dc.subject | sulfite | en_US |
dc.subject | sulfite oxidase | en_US |
dc.subject | superoxide dismutase | en_US |
dc.subject | thiobarbituric acid reactive substance | en_US |
dc.subject | tungsten | en_US |
dc.subject | antioxidant | en_US |
dc.subject | food preservative | en_US |
dc.subject | animal cell | en_US |
dc.subject | animal experiment | en_US |
dc.subject | article | en_US |
dc.subject | controlled study | en_US |
dc.subject | defense mechanism | en_US |
dc.subject | enzyme activity | en_US |
dc.subject | enzyme deficiency | en_US |
dc.subject | erythrocyte | en_US |
dc.subject | hemolysate | en_US |
dc.subject | lipid peroxidation | en_US |
dc.subject | male | en_US |
dc.subject | nonhuman | en_US |
dc.subject | oxidation | en_US |
dc.subject | rat | en_US |
dc.subject | animal | en_US |
dc.subject | drug effect | en_US |
dc.subject | metabolism | en_US |
dc.subject | Wistar rat | en_US |
dc.subject | Animalia | en_US |
dc.subject | Rattus | en_US |
dc.subject | Animals | en_US |
dc.subject | Catalase | en_US |
dc.subject | Erythrocytes | en_US |
dc.subject | Food Preservatives | en_US |
dc.subject | Glucosephosphate Dehydrogenase | en_US |
dc.subject | Glutathione Peroxidase | en_US |
dc.subject | Lipid Peroxidation | en_US |
dc.subject | Rats | en_US |
dc.subject | Rats, Wistar | en_US |
dc.subject | Sulfite Oxidase | en_US |
dc.subject | Sulfites | en_US |
dc.subject | Superoxide Dismutase | en_US |
dc.subject | Thiobarbituric Acid Reactive Substances | en_US |
dc.title | Effect of sulfite on antioxidant enzymes and lipid peroxidation in normal and sulfite oxidase-deficient rat erythrocytes | en_US |
dc.type | Article | en_US |
dc.identifier.volume | 66 | en_US |
dc.identifier.issue | 3 | en_US |
dc.identifier.startpage | 205 | |
dc.identifier.startpage | 205 | en_US |
dc.identifier.endpage | 212 | en_US |
dc.authorid | 0000-0002-6850-6281 | - |
dc.identifier.doi | 10.1007/s13105-010-0025-7 | - |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.identifier.pmid | 20571963 | en_US |
dc.identifier.scopus | 2-s2.0-78349303088 | en_US |
dc.identifier.wos | WOS:000284061300003 | en_US |
dc.identifier.scopusquality | Q2 | - |
dc.owner | Pamukkale University | - |
item.fulltext | No Fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.cerifentitytype | Publications | - |
item.languageiso639-1 | en | - |
item.grantfulltext | none | - |
item.openairetype | Article | - |
crisitem.author.dept | 14.03. Basic Medical Sciences | - |
Appears in Collections: | PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection Tıp Fakültesi Koleksiyonu WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection |
CORE Recommender
SCOPUSTM
Citations
20
checked on Nov 16, 2024
WEB OF SCIENCETM
Citations
19
checked on Nov 15, 2024
Page view(s)
56
checked on Aug 24, 2024
Google ScholarTM
Check
Altmetric
Items in GCRIS Repository are protected by copyright, with all rights reserved, unless otherwise indicated.