Lipid peroxidation in the etiology of alcohol liver injury and cancer: Modulatory role of vitamin E.

Persistent Link:
http://hdl.handle.net/10150/185566
Title:
Lipid peroxidation in the etiology of alcohol liver injury and cancer: Modulatory role of vitamin E.
Author:
Odeleye, Olalekan Elufisayo.
Issue Date:
1991
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
The role of increased lipid peroxidation (LP) as the operative mechanism in the early and later stages in the development of alcoholic liver injuries and cancer were investigated. Adult male rats were fed liquid diets containing 36% as ethanol derived calories, with cod liver oil substituting for corn oil, olive oil and cotton seed oil (n-6 fatty acid) for 28 days or 18 months. Control rats received similar diets supplemented with vitamin E. Indices of increased LP including elevated hepatic conjugated dienes, lipid fluorescence, malondialdehyde and ethane exhalation were observed in rats fed ethanol and cod liver oil. These changes were significantly reduced by supplemental vitamin V. Similarly, changes in major components of the membrane lipids, peroxidation of hepatic PUFA and depleted levels of hepatic vitamin A and E were partially reversed in the vitamin E supplemented animals. Thus, increased LP, attenuated by dietary vitamin E, is an attendant mechanism in alcoholic liver injury. In other experiments, female C57BL/6 mice were treated with or without ethanol, cocaine, LP-BM5 murine leukemia retrovirus, low protein diets, methylbenzylnitrosamine and supplemental vitamin E. Ethanol suppressed the numbers of T-cell, macrophages and increased the accumulation of indices of increased LP. Significant increases in T-subsets, B-cells and macrophages were observed in the retrovirus infected animals. These changes were further exacerbated in the virus infected animals exposed to ethanol. Similarly, exposure to ethanol in cocaine treated animals synergistically increased cocaine-induced lipid peroxidation. Furthermore, increased products of LP and severe liver pathologic damages were seen in immunocompromised animals fed low levels of dietary protein treated with cocaine. Additionally, exposure to ethanol promoted the size and frequency of chemically-induced esophageal preneoplastic tumor via an attendant increased LP. Supplemental dietary vitamin E reduced the indices of LP and the size and frequency of the preneoplastic tumors. Thus, increased LP, attenuated by dietary vitamin E, is an attendant mechanism in the complex process of carcinogenesis induced by a chemical carcinogen, and promoted by ethanol, protein malnutrition and retrovirus infection.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Dissertations, Academic; Biochemistry; Nutrition; Pathology.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Nutritional Sciences; Graduate College
Degree Grantor:
University of Arizona
Advisor:
Watson, Ronald R.

Full metadata record

DC FieldValue Language
dc.language.isoenen_US
dc.titleLipid peroxidation in the etiology of alcohol liver injury and cancer: Modulatory role of vitamin E.en_US
dc.creatorOdeleye, Olalekan Elufisayo.en_US
dc.contributor.authorOdeleye, Olalekan Elufisayo.en_US
dc.date.issued1991en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractThe role of increased lipid peroxidation (LP) as the operative mechanism in the early and later stages in the development of alcoholic liver injuries and cancer were investigated. Adult male rats were fed liquid diets containing 36% as ethanol derived calories, with cod liver oil substituting for corn oil, olive oil and cotton seed oil (n-6 fatty acid) for 28 days or 18 months. Control rats received similar diets supplemented with vitamin E. Indices of increased LP including elevated hepatic conjugated dienes, lipid fluorescence, malondialdehyde and ethane exhalation were observed in rats fed ethanol and cod liver oil. These changes were significantly reduced by supplemental vitamin V. Similarly, changes in major components of the membrane lipids, peroxidation of hepatic PUFA and depleted levels of hepatic vitamin A and E were partially reversed in the vitamin E supplemented animals. Thus, increased LP, attenuated by dietary vitamin E, is an attendant mechanism in alcoholic liver injury. In other experiments, female C57BL/6 mice were treated with or without ethanol, cocaine, LP-BM5 murine leukemia retrovirus, low protein diets, methylbenzylnitrosamine and supplemental vitamin E. Ethanol suppressed the numbers of T-cell, macrophages and increased the accumulation of indices of increased LP. Significant increases in T-subsets, B-cells and macrophages were observed in the retrovirus infected animals. These changes were further exacerbated in the virus infected animals exposed to ethanol. Similarly, exposure to ethanol in cocaine treated animals synergistically increased cocaine-induced lipid peroxidation. Furthermore, increased products of LP and severe liver pathologic damages were seen in immunocompromised animals fed low levels of dietary protein treated with cocaine. Additionally, exposure to ethanol promoted the size and frequency of chemically-induced esophageal preneoplastic tumor via an attendant increased LP. Supplemental dietary vitamin E reduced the indices of LP and the size and frequency of the preneoplastic tumors. Thus, increased LP, attenuated by dietary vitamin E, is an attendant mechanism in the complex process of carcinogenesis induced by a chemical carcinogen, and promoted by ethanol, protein malnutrition and retrovirus infection.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectDissertations, Academicen_US
dc.subjectBiochemistryen_US
dc.subjectNutritionen_US
dc.subjectPathology.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplineNutritional Sciencesen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorWatson, Ronald R.en_US
dc.contributor.committeememberUdall, Johnen_US
dc.contributor.committeememberPrice, Ralphen_US
dc.contributor.committeememberEskelson, Cleamond D.en_US
dc.contributor.committeememberEarnest, Daviden_US
dc.identifier.proquest9200019en_US
dc.identifier.oclc711708546en_US
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