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Cited by 267Neutrophil, Myeloperoxidase and Oxidative MechanismsAtherosclerosis and Cardiovascular DiseasesAntioxidant Activity and Oxidative Stress

The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.

Oxidation of low-density lipoprotein by hypochlorite causes aggregation that is mediated by modification of lysine residues rather than lipid oxidation

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Hazell, L J, van den Berg, J J M, Stocker, R·1994·Biochemical Journal
DOI 10.1042/bj3020297PMC PMC1137223
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Abstract

Peroxidation of low-density lipoprotein (LDL) lipid is generally thought to represent the initial step in a series of modification reactions that ultimately transform the protein moiety of the lipoprotein into a form recognized by receptors different from those that bind native LDL. Uptake of LDL via these alternative receptors can lead to the formation of lipid-laden cells, which are typical for the early stages of atherogenesis. We have studied the oxidative modification of LDL by hypochlorite (-OCl), a powerful oxidant produced from H2O2 and chloride via the action of myeloperoxidase which is released from activated neutrophils and monocytes. Exposure of LDL to reagent or enzymically generated -OCl at 4 or 37 degrees C resulted in immediate and preferential oxidation of amino acid residues of apolipoprotein B-100, the single protein associated with LDL. Lysine residues quantitatively represented the major target and, like tryptophan, were oxidized to approximately the same extent with reagent or enzymically generated -OCl. In contrast, LDL lipid oxidation was less favoured than protein oxidation, as judged by the amounts of lipid hydroperoxides, chlorohydrins, cholesterol or fatty acid oxidation products formed. Treatment with -OCl caused aggregation of LDL, as shown by an increased turbidity of the oxidized LDL solution and elution from a size-exclusion h.p.l.c. column of high-molecular-mass LDL complexes. Chemical modification of lysine residues before oxidation with -OCl prevented aggregation, while it enhanced the extent of lipid peroxidation. Treatment of LDL with -OCl also caused the formation of carbonyl groups and release of ammonia; both these modifications were inhibited by lysine-residue modification before oxidation. These results demonstrate that aggregation reactions are dependent on initial lysine oxidation by -OCl, followed by deamination and carbonyl formation, but do not involve lipid (per)oxidation. We propose that the observed -OCl-mediated aggregation of LDL is caused, at least in part, by cross-linking of apoproteins by Schiff-base formation independently of lipid peroxidation.

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Metadata

Authors
Hazell, L. J., van den Berg, J. J. M., & Stocker, R.
Affiliations
  • The Heart Research Institute (AU)
  • Children's Hospital Oakland Research Institute, Oakland, CA 94609, U.S.
Corresponding author
Stocker, R
ORCID
Stocker, R
Venue
Biochemical Journal
Publisher
Portland Press Ltd.
Published
1994-08-15
Volume
302
Issue
1
Pages
297-304
ISSN
  • 0264-6021 (ISSN-L)
  • 1470-8728
DOI
10.1042/bj3020297
PMC
PMC1137223
OpenAlex
W2142527036
Cited by
267
References
44
Citations by year
2025: 2 · 2024: 4 · 2023: 5 · 2022: 3 · 2021: 6 · 2020: 7 · 2019: 4 · 2018: 6 · 2017: 5 · 2016: 11 · 2015: 5 · 2014: 6 · 2013: 7 · 2012: 9
FWCI
5.61
Type
journal article
Language
en
Open access
Locations
  • Biochemical Journal (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • U.S. Department of Health and Human Services
  • Tobacco-Related Disease Research Program
  • National Institutes of Health (5r01dk034400-10)
  • Medical Research Council
  • National Health and Medical Research Council
  • National Institute of Diabetes and Digestive and Kidney Diseases (P01DK032094, DK-34400, DK32094)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
Keywords
LDL oxidation, hypochlorite, lysine oxidation, LDL aggregation, apolipoprotein B-100, lipid peroxidation, myeloperoxidase, atherogenesis, Schiff base formation, protein cross-linking, carbonyl formation, tryptophan oxidation, lipid hydroperoxides, neutrophils, monocytes
MeSH terms
Adult, Female, Humans, Hypochlorous Acid, Lipoproteins, LDL, Lysine, Male, Oxidation-Reduction

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