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- Publisher Website: 10.1007/BF00926919
- Scopus: eid_2-s2.0-0028129217
- PMID: 7969093
- WOS: WOS:A1994NT09500003
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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
Title | Effects of selenium and α-tocopherol on liver damage induced by feeding grains from an endemic area of Keshan disease in rats |
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Authors | |
Keywords | α-tocopherol Keshan disease lipid peroxidation liver damage rat selenium |
Issue Date | 1994 |
Publisher | Springer 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? |
Abstract | Previous 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 Identifier | http://hdl.handle.net/10722/171127 |
ISSN | 2023 Impact Factor: 3.5 2023 SCImago Journal Rankings: 0.901 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Liu, SY | en_US |
dc.contributor.author | Li, TY | en_US |
dc.contributor.author | Zhao, Z | en_US |
dc.contributor.author | Man, RYK | en_US |
dc.contributor.author | Wang, F | en_US |
dc.date.accessioned | 2012-10-30T06:12:18Z | - |
dc.date.available | 2012-10-30T06:12:18Z | - |
dc.date.issued | 1994 | en_US |
dc.identifier.citation | Molecular And Cellular Biochemistry, 1994, v. 132 n. 2, p. 109-115 | en_US |
dc.identifier.issn | 0300-8177 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171127 | - |
dc.description.abstract | Previous 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.language | eng | en_US |
dc.publisher | Springer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0300-8177 | en_US |
dc.relation.ispartof | Molecular and Cellular Biochemistry | en_US |
dc.subject | α-tocopherol | - |
dc.subject | Keshan disease | - |
dc.subject | lipid peroxidation | - |
dc.subject | liver damage | - |
dc.subject | rat | - |
dc.subject | selenium | - |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Cardiomyopathies - Etiology - Prevention & Control | en_US |
dc.subject.mesh | Cereals | en_US |
dc.subject.mesh | Histocytochemistry | en_US |
dc.subject.mesh | Liver Diseases - Enzymology - Etiology - Prevention & Control | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Rats | en_US |
dc.subject.mesh | Rats, Wistar | en_US |
dc.subject.mesh | Selenium - Deficiency - Pharmacology | en_US |
dc.subject.mesh | Vitamin E - Pharmacology | en_US |
dc.title | Effects of selenium and α-tocopherol on liver damage induced by feeding grains from an endemic area of Keshan disease in rats | en_US |
dc.type | Article | en_US |
dc.identifier.email | Man, RYK:rykman@hkucc.hku.hk | en_US |
dc.identifier.authority | Man, RYK=rp00236 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1007/BF00926919 | en_US |
dc.identifier.pmid | 7969093 | - |
dc.identifier.scopus | eid_2-s2.0-0028129217 | en_US |
dc.identifier.volume | 132 | en_US |
dc.identifier.issue | 2 | en_US |
dc.identifier.spage | 109 | en_US |
dc.identifier.epage | 115 | en_US |
dc.identifier.isi | WOS:A1994NT09500003 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Liu, SY=24822482600 | en_US |
dc.identifier.scopusauthorid | Li, TY=16413269500 | en_US |
dc.identifier.scopusauthorid | Zhao, Z=8262522900 | en_US |
dc.identifier.scopusauthorid | Man, RYK=7004986435 | en_US |
dc.identifier.scopusauthorid | Wang, F=7501310980 | en_US |
dc.identifier.issnl | 0300-8177 | - |