Mechanisms of homocysteine toxicity in humans

Homocysteine, a non-protein amino acid, is an important risk factor for ischemic heart disease and stroke in humans. This review provides an overview of homocysteine influence on endothelium function as well as on protein metabolism with a special respect to posttranslational modification of protein...

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Bibliographic Details
Published in:Amino acids 2007-05, Vol.32 (4), p.561-572
Main Authors: Perła-Kaján, J, Twardowski, T, Jakubowski, H
Format: Article
Language:English
Subjects:
Amides
Amino acids
Animals
Aryldialkylphosphatase - metabolism
autoantibodies
Disulfides
Heart diseases
Hemostasis
Homocysteine
Homocysteine - analogs & derivatives
Homocysteine - chemistry
Homocysteine - metabolism
Homocysteine thiolactone
Homocystine - blood
Homocystine - chemistry
Homocystine - metabolism
Human
Humans
Hyperhomocysteinemia - metabolism
Hyperhomocysteinemia - physiopathology
Inducers
Inflammation - metabolism
Lipoproteins, HDL - metabolism
Lipoproteins, LDL - metabolism
Protein N-homocysteinylation
Protein S-homocysteinylation
Protein-Lysine 6-Oxidase - antagonists & inhibitors
Protein-Lysine 6-Oxidase - metabolism
Proteins
Proteins - immunology
Proteins - metabolism
Toxicity
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Summary:Homocysteine, a non-protein amino acid, is an important risk factor for ischemic heart disease and stroke in humans. This review provides an overview of homocysteine influence on endothelium function as well as on protein metabolism with a special respect to posttranslational modification of protein with homocysteine thiolactone. Homocysteine is a pro-thrombotic factor, vasodilation impairing agent, pro-inflammatory factor and endoplasmatic reticulum-stress inducer. Incorporation of Hcy into protein via disulfide or amide linkages (S-homocysteinylation or N-homocysteinylation) affects protein structure and function. Protein N-homocysteinylation causes cellular toxicity and elicits autoimmune response, which may contribute to atherogenesis.
ISSN:0939-4451
1438-2199
DOI:10.1007/s00726-006-0432-9