Oxidative stress and atherosclerosis

T. T C Yang, S. Devaraj, I. Jialal

Research output: Contribution to journalArticle

19 Scopus citations

Abstract

Cardiovascular disease is the leading cause of death in westernized populations. Accumulating evidence suggests that lipid peroxidation is pivotal in atherogenesis. Supplementation with antioxidants, e.g., vitamin E, has been shown in animal models and humans to reduce atherosclerotic lesion progression and cardiovascular events. Methods to evaluate oxidative stress include direct and indirect measures. The most relevant direct measure of oxidative stress is urinary F2-isoprostanes, which are prostaglandin-like compounds formed in vivo from free radical catalyzed peroxidation of arachidonic acid via a non-cycloxygenase-dependent mechanism. The measurement of F2-isoprostanes provides a sensitive, specific, and non-invasive method for the assessment of in vivo lipid peroxidation. Other direct measures include autoantibodies to oxidized LDL, and assaying modified LDL in plasma, breath volatile hydrocarbons, and protein carbonyl. Measures of autoantibodies and modified LDL still need further standardization before they can be specific and sensitive direct measures of oxidative stress. Indirect measures of oxidative stress include measurement of total antioxidant capacity (ORAC, TRAP), individual antioxidant status (including glutathione, alpha-tocopherol, carotenoids, and ascorbate) and LDL oxidizability (including conjugated dienes, lipid peroxides, TBARS, apo B-100 fluorescence, and fatty acid content).

Original languageEnglish (US)
Pages (from-to)13-24
Number of pages12
JournalJournal of Clinical Ligand Assay
Volume24
Issue number1
StatePublished - 2001
Externally publishedYes

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Keywords

  • Alpha-tocopherol
  • Antioxidant
  • Atherosclerosis
  • F-isoprostanes
  • Low density lipoprotein
  • Oxidative stress

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Immunology

Cite this

Yang, T. T. C., Devaraj, S., & Jialal, I. (2001). Oxidative stress and atherosclerosis. Journal of Clinical Ligand Assay, 24(1), 13-24.