Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Postprandial oxidative stress.

Fulvio Ursini1, Alex Sevanian

  • 1Department of Biological Chemistry, University of Padova, Italy.

Biological Chemistry
|May 30, 2002
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

A thermodynamic constraint on GPx4 flux links glutathione redox state to ferroptotic commitment.

Free radical biology & medicine·2026
Same author

Cardiolipin drives the catalytic activity of GPX4 on membranes: Insights from the R152H mutant.

Redox biology·2023
Same author

A white paper on Phospholipid Hydroperoxide Glutathione Peroxidase (GPx4) forty years later.

Free radical biology & medicine·2022
Same author

Fifty years of selenoenzyme research: Discoveries, state-of-the-art and future directions.

Free radical biology & medicine·2022
Same author

Hydrogen peroxide signaling via its transformation to a stereospecific alkyl hydroperoxide that escapes reductive inactivation.

Nature communications·2021
Same author

Production and purification of homogenous recombinant human selenoproteins reveals a unique codon skipping event in E. coli and GPX4-specific affinity to bromosulfophthalein.

Redox biology·2021

Eating meals with oxidized fats increases harmful lipid hydroperoxides and LDL oxidation, raising atherosclerosis risk. Antioxidants, like those in red wine, can protect against this postprandial oxidative stress.

Area of Science:

  • Nutritional Science
  • Cardiovascular Research
  • Biochemistry

Background:

  • Postprandial lipid oxidation can increase plasma lipid hydroperoxides.
  • This process enhances low-density lipoprotein (LDL) susceptibility to oxidation.
  • Oxidized lipids may cause structural changes in LDL particles.

Purpose of the Study:

  • To investigate the effects of consuming a meal with oxidized lipids on plasma lipid hydroperoxides and LDL oxidation.
  • To identify the role of LDL- (a subfraction of LDL) in postprandial LDL modification.
  • To assess the protective effects of antioxidants against meal-induced oxidative stress.

Main Methods:

  • Measurement of plasma lipid hydroperoxides using chemiluminescence.
  • Assessment of LDL susceptibility to oxidation postprandially.

Related Experiment Videos

  • Characterization of LDL subfractions, including LDL- containing denatured apoprotein-B-100 (apoB-100).
  • Main Results:

    • Meal consumption led to increased plasma lipid hydroperoxides and LDL oxidation.
    • An increase in LDL- was observed postprandially, associated with denatured apoB-100.
    • Antioxidants, such as those in red wine, mitigated postprandial oxidative stress and LDL modification.

    Conclusions:

    • Postprandial lipid oxidation contributes to LDL modification and increases susceptibility to oxidation.
    • Antioxidant consumption can inhibit lipid peroxidation, protecting LDL from oxidative damage.
    • In vivo oxidatively modified LDL shares characteristics with atherogenic LDL, linking nutrition to atherosclerosis development.