Protective Effects of Selenium, N-Acetylcysteine and Vitamin E Against Acute Ethanol Intoxication in Rats

dc.contributor.author Ozkol, Halil
dc.contributor.author Bulut, Gulay
dc.contributor.author Balahoroglu, Ragip
dc.contributor.author Tuluce, Yasin
dc.contributor.author Ozkol, Hatice Uce
dc.date.accessioned 2025-05-10T17:40:36Z
dc.date.available 2025-05-10T17:40:36Z
dc.date.issued 2017
dc.description Tuluce, Yasin/0000-0002-7312-5934 en_US
dc.description.abstract The aim of this study was to determine possible protective influences of selenium (Se), N-acetylcysteine (NAC), and vitamin E (Vit E) against acute ethanol (EtOH) intoxication. Thirty-six rats were divided into six groups: I (control), II (EtOH), III (EtOH + Se), IV (EtOH + Vit E), V (EtOH + NAC), and VI (EtOH + mix). Except group I, EtOH was given the other pretreated (groups III, IV, V, and VI) and untreated groups (group II). Compared with the EtOH group, serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, lactate dehydrogenase, creatine kinase, and creatine kinase-MB levels were significantly decreased in all pretreated groups, whereas slightly diminished amylase and lipase were observed. Compared with the control group, a remarkably lower total antioxidant status (TAS), but higher total oxidant status (TOS), and oxidative stress index (OSI) were seen in brain, liver, and kidney tissues. The values of these parameters were less affected from EtOH-exposed brain tissue of EtOH + NAC and liver of EtOH + mix groups. Both significant decrease of catalase activity and marked increases of adenosine deaminase and myeloperoxidase were determined only in liver tissue of the EtOH group. Activities of these enzymes were restored in almost all pretreated groups. Moreover, an increase of xanthine oxidase activity was prevented in brain tissue of pretreated groups. In histopathological examination of the liver, hydropic degeneration, sinusoidal dilatation, mononuclear cell infiltration, and marked congestion, which were seen in the EtOH group, were prevented in all pretreated groups. Relative protection against acute EtOH toxicity, in both single and combined pretreatments of Se, NAC, and Vit E supplementation, was probably through antioxidant and free radical-neutralizing effects of foregoing materials. en_US
dc.identifier.doi 10.1007/s12011-016-0762-8
dc.identifier.issn 0163-4984
dc.identifier.issn 1559-0720
dc.identifier.scopus 2-s2.0-84973151749
dc.identifier.uri https://doi.org/10.1007/s12011-016-0762-8
dc.identifier.uri https://hdl.handle.net/20.500.14720/15255
dc.language.iso en en_US
dc.publisher Springernature en_US
dc.rights info:eu-repo/semantics/closedAccess en_US
dc.subject Acute Ethanol Toxicity en_US
dc.subject Selenium en_US
dc.subject N-Acetylcysteine en_US
dc.subject Vitamin E en_US
dc.subject Rat en_US
dc.title Protective Effects of Selenium, N-Acetylcysteine and Vitamin E Against Acute Ethanol Intoxication in Rats en_US
dc.type Article en_US
dspace.entity.type Publication
gdc.author.id Tuluce, Yasin/0000-0002-7312-5934
gdc.author.scopusid 36574004100
gdc.author.scopusid 26646261000
gdc.author.scopusid 6507988055
gdc.author.scopusid 10143414500
gdc.author.scopusid 54179576500
gdc.author.wosid Tuluce, Yasin/S-6812-2016
gdc.coar.access metadata only access
gdc.coar.type text::journal::journal article
gdc.description.department T.C. Van Yüzüncü Yıl Üniversitesi en_US
gdc.description.departmenttemp [Ozkol, Halil; Tuluce, Yasin] Yuzuncu Yil Univ, Dept Med Biol, Fac Med, Van, Turkey; [Bulut, Gulay] Yuzuncu Yil Univ, Dept Pathol, Fac Med, Van, Turkey; [Balahoroglu, Ragip] Yuzuncu Yil Univ, Dept Biochem, Fac Med, Van, Turkey; [Ozkol, Hatice Uce] Yuzuncu Yil Univ, Dept Dermatol, Fac Med, Van, Turkey en_US
gdc.description.endpage 185 en_US
gdc.description.issue 1 en_US
gdc.description.publicationcategory Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı en_US
gdc.description.scopusquality Q1
gdc.description.startpage 177 en_US
gdc.description.volume 175 en_US
gdc.description.woscitationindex Science Citation Index Expanded
gdc.description.wosquality Q2
gdc.identifier.pmid 27250492
gdc.identifier.wos WOS:000392194700023
gdc.index.type WoS
gdc.index.type Scopus
gdc.index.type PubMed

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