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Acetaminophen-induced toxicity is prevented by beta-D-glucan treatment in mice

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dc.contributor.authorVELİOĞLU ÖĞÜNÇ, AYLİZ
dc.contributor.authorsToklu, Hale Z.; Sehirli, A. Ozer; Velioglu-Ogunc, Ayliz; Cetinel, Sule; Sener, Goksel
dc.date.accessioned2022-03-12T17:18:41Z
dc.date.available2022-03-12T17:18:41Z
dc.date.issued2006
dc.description.abstractThe protective effect of beta-glucan against oxidative injury caused by acetaminophen was studied in mice liver. BALB-c mice (25-30 g) were pretreated with beta-D-glucan (50 mg/kg, p.o.) for 10 days and on the 11th day they received an overdose of acetaminophen (900 mg/kg, i.p.). Four hours after the acetaminophen injection, mice were decapitated and their blood was taken to determine serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) and tumor necrosis factor-alpha (TNF-alpha) levels. Tissue samples of the liver were taken for histological examination or for the determination of levels of malondialdehyde, an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and myeloperoxidase activity, an index of tissue neutrophil infiltration. The formation of reactive oxygen species in hepatic tissue samples was monitored by using the chemilummescence technique with luminol and lucigenin probes. Acetaminophen caused a significant decrease in the GSH level of the tissue, which was accompanied with significant increases in the hepatic luminol and lucigenin chemiluminescence values, malondialdehyde level, MPO activity and collagen content. Similarly, serum ALT, AST levels, as well as LDH and TNF-alpha, were elevated in the acetaminophen-treated group when compared with the control group. On the other hand, P-D-glucan treatment reversed all these biochemical indices, as well as histopathological alterations that were induced by acetaminophen. In conclusion, these results suggest that beta-D-glucan exerts cytoprotective effects against oxidative injury through its antioxidant properties and may be of therapeutic use in preventing acetaminophen toxicity. (c) 2006 Elsevier B.V. All rights reserved.
dc.identifier.doi10.1016/j.ejphar.2006.05.033
dc.identifier.issn0014-2999
dc.identifier.pubmed16822497
dc.identifier.urihttps://hdl.handle.net/11424/227999
dc.identifier.wosWOS:000239684700019
dc.language.isoeng
dc.publisherELSEVIER SCIENCE BV
dc.relation.ispartofEUROPEAN JOURNAL OF PHARMACOLOGY
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectacetaminophen
dc.subjectbeta-glucan
dc.subjectglutathione
dc.subjectlipid peroxidation
dc.subjectoxidative injury
dc.subjecttumour necrosis factor-alpha
dc.subjectSTAPHYLOCOCCAL WOUND-INFECTION
dc.subjectINDUCED LIPID-PEROXIDATION
dc.subjectGUINEA-PIG MODEL
dc.subjectSUPEROXIDE ANION
dc.subjectOXIDATIVE STRESS
dc.subjectCYTOKINE RELEASE
dc.subjectREACTIVE OXYGEN
dc.subjectPROTECTIVE ROLE
dc.subjectFREE-RADICALS
dc.subjectIN-VITRO
dc.titleAcetaminophen-induced toxicity is prevented by beta-D-glucan treatment in mice
dc.typearticle
dspace.entity.typePublication
local.avesis.idfc9d3a8b-73cf-4da8-98d6-40b2a1a1788e
local.import.packageSS17
local.indexed.atWOS
local.indexed.atSCOPUS
local.indexed.atPUBMED
local.journal.numberofpages8
oaire.citation.endPage140
oaire.citation.issue1-3
oaire.citation.startPage133
oaire.citation.titleEUROPEAN JOURNAL OF PHARMACOLOGY
oaire.citation.volume543
relation.isAuthorOfPublication13300bf6-ba96-4f87-9868-b0d2c86f572a
relation.isAuthorOfPublication.latestForDiscovery13300bf6-ba96-4f87-9868-b0d2c86f572a

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