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Article: Effects of selenium and α-tocopherol on liver damage induced by feeding grains from an endemic area of Keshan disease in rats

TitleEffects of selenium and α-tocopherol on liver damage induced by feeding grains from an endemic area of Keshan disease in rats
Authors
Issue Date1994
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0300-8177
Citation
Molecular And Cellular Biochemistry, 1994, v. 132 n. 2, p. 109-115 How to Cite?
AbstractPrevious studies have shown the pathogenic effects of grains cultivated in the endemic areas of Keshan disease and selenium is effective in the prevention of this disease. In this study, liver damages induced by feeding grains from an endemic area (endemic diet), and the effects of selenium and α-tocopherol supplement were examined. After 3 months on the endemic diet, the amounts of serum enzymes were significantly increased when compared to controls (animals receiving diet from a non-endemic area). Liver enzymes (alkaline phosphatase and choline esterase) were also found to be altered in the serum, further suggesting liver damages in animals on an endemic diet. Supplement of the endemic diet with selenium or α-tocopherol reversed the changes in serum enzymes. Increase in lipid peroxidation in the liver of animals on the endemic diet was observed when compared to that in control animals. Selenium and α-tocopherol supplements prevented the increase in lipid peroxidation in the liver by the endemic diet. Semi-quantitative histochemical analysis of glutamate dehydrogenase and succinate dehydrogenase in liver tissue showed that the livers of animals on an endemic diet were more sensitive to ischemic damages in vitro. Supplementation of the endemic diet with either selenium or α-tocopherol reduced the sensitivity to ischemic damages. The results suggest that increased lipid peroxidation in the liver of rats on an endemic diet may be responsible for liver damages and elevation of serum enzymes. Restoration of glutathione peroxidase activity by selenium supplement or an increase in the content of α-tocopherol in the liver can prevent lipid peroxidation in animals on an endemic diet and thus provide the protective effects against liver damages.
Persistent Identifierhttp://hdl.handle.net/10722/171127
ISSN
2015 Impact Factor: 2.613
2015 SCImago Journal Rankings: 1.019
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLiu, SYen_US
dc.contributor.authorLi, TYen_US
dc.contributor.authorZhao, Zen_US
dc.contributor.authorMan, RYKen_US
dc.contributor.authorWang, Fen_US
dc.date.accessioned2012-10-30T06:12:18Z-
dc.date.available2012-10-30T06:12:18Z-
dc.date.issued1994en_US
dc.identifier.citationMolecular And Cellular Biochemistry, 1994, v. 132 n. 2, p. 109-115en_US
dc.identifier.issn0300-8177en_US
dc.identifier.urihttp://hdl.handle.net/10722/171127-
dc.description.abstractPrevious studies have shown the pathogenic effects of grains cultivated in the endemic areas of Keshan disease and selenium is effective in the prevention of this disease. In this study, liver damages induced by feeding grains from an endemic area (endemic diet), and the effects of selenium and α-tocopherol supplement were examined. After 3 months on the endemic diet, the amounts of serum enzymes were significantly increased when compared to controls (animals receiving diet from a non-endemic area). Liver enzymes (alkaline phosphatase and choline esterase) were also found to be altered in the serum, further suggesting liver damages in animals on an endemic diet. Supplement of the endemic diet with selenium or α-tocopherol reversed the changes in serum enzymes. Increase in lipid peroxidation in the liver of animals on the endemic diet was observed when compared to that in control animals. Selenium and α-tocopherol supplements prevented the increase in lipid peroxidation in the liver by the endemic diet. Semi-quantitative histochemical analysis of glutamate dehydrogenase and succinate dehydrogenase in liver tissue showed that the livers of animals on an endemic diet were more sensitive to ischemic damages in vitro. Supplementation of the endemic diet with either selenium or α-tocopherol reduced the sensitivity to ischemic damages. The results suggest that increased lipid peroxidation in the liver of rats on an endemic diet may be responsible for liver damages and elevation of serum enzymes. Restoration of glutathione peroxidase activity by selenium supplement or an increase in the content of α-tocopherol in the liver can prevent lipid peroxidation in animals on an endemic diet and thus provide the protective effects against liver damages.en_US
dc.languageengen_US
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0300-8177en_US
dc.relation.ispartofMolecular and Cellular Biochemistryen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCardiomyopathies - Etiology - Prevention & Controlen_US
dc.subject.meshCerealsen_US
dc.subject.meshHistocytochemistryen_US
dc.subject.meshLiver Diseases - Enzymology - Etiology - Prevention & Controlen_US
dc.subject.meshMaleen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshSelenium - Deficiency - Pharmacologyen_US
dc.subject.meshVitamin E - Pharmacologyen_US
dc.titleEffects of selenium and α-tocopherol on liver damage induced by feeding grains from an endemic area of Keshan disease in ratsen_US
dc.typeArticleen_US
dc.identifier.emailMan, RYK:rykman@hkucc.hku.hken_US
dc.identifier.authorityMan, RYK=rp00236en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1007/BF00926919en_US
dc.identifier.pmid7969093-
dc.identifier.scopuseid_2-s2.0-0028129217en_US
dc.identifier.volume132en_US
dc.identifier.issue2en_US
dc.identifier.spage109en_US
dc.identifier.epage115en_US
dc.identifier.isiWOS:A1994NT09500003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLiu, SY=24822482600en_US
dc.identifier.scopusauthoridLi, TY=16413269500en_US
dc.identifier.scopusauthoridZhao, Z=8262522900en_US
dc.identifier.scopusauthoridMan, RYK=7004986435en_US
dc.identifier.scopusauthoridWang, F=7501310980en_US

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