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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
1997-10-20
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pubmed:abstractText |
Captopril ([2S]-1-[3-mercapto-2-methyl-propionyl]-L-proline) was found to protect erythrocytes from hemolysis caused by 2,2'-azobis (2-amidinopropane) (AAPH) and hypochlorite, erythrocyte membranes from lipid peroxidation caused by tert-butyl hydroperoxide (tBOOH) and hypochlorite, erythrocyte membrane ATPases from inactivation caused by tBOOH and hemoglobin from oxidation caused by AAPH and tBOOH. In all these systems enalapril ([S]-1-[N-(1-[ethoxycarbonyl]-3-phenylpropyl)-L-alanyl]-L-proline) was not protective or even increased the damage, especially with hypochlorite, probably due to chloramine formation. Captopril but not enalapril inhibited ascorbate autoxidation caused by Cu2+, which indicates that captopril binds Cu2+. On the other hand, deoxyribose degradation caused by iron and copper ions and DNA damage by o-phenanthroline/Cu2+/H2O2/beta-mercaptoethanol was enhanced by both captopril and enalapril. The effect of captopril was usually higher, apparently due to the reducing properties of captopril, which could reduce metal ions enabling their participation in the Fenton reaction. These results indicate that only -SH-group-containing inhibitors of angiotensin-converting enzyme (ACE) may exhibit antioxidant properties, and that the antioxidant/prooxidant action of ACE inhibitors depends on the system studied in vitro.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphatases,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin-Converting Enzyme...,
http://linkedlifedata.com/resource/pubmed/chemical/Antioxidants,
http://linkedlifedata.com/resource/pubmed/chemical/Ascorbic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Captopril,
http://linkedlifedata.com/resource/pubmed/chemical/Deoxyribose,
http://linkedlifedata.com/resource/pubmed/chemical/Enalapril
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pubmed:status |
MEDLINE
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pubmed:issn |
0891-5849
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
23
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
729-35
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:9296449-Adenosine Triphosphatases,
pubmed-meshheading:9296449-Angiotensin-Converting Enzyme Inhibitors,
pubmed-meshheading:9296449-Antioxidants,
pubmed-meshheading:9296449-Ascorbic Acid,
pubmed-meshheading:9296449-Captopril,
pubmed-meshheading:9296449-DNA Damage,
pubmed-meshheading:9296449-Deoxyribose,
pubmed-meshheading:9296449-Enalapril,
pubmed-meshheading:9296449-Erythrocyte Membrane,
pubmed-meshheading:9296449-Hemolysis,
pubmed-meshheading:9296449-Humans,
pubmed-meshheading:9296449-Lipid Peroxidation,
pubmed-meshheading:9296449-Oxidation-Reduction
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pubmed:year |
1997
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pubmed:articleTitle |
Antioxidant and prooxidant properties of captopril and enalapril.
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pubmed:affiliation |
Department of Physiology, Institute of Fundamental Sciences, Military Medical University, Lód?, Poland.
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pubmed:publicationType |
Journal Article,
Comparative Study
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