ArticleAntioxidants & redox signaling2009
Alpha-tocopherol is ineffective in preventing the decomposition of preformed lipid peroxides and may promote the accumulation of toxic aldehydes: a potential explanation for the failure of antioxidants to affect human atherosclerosis.
Article in Antioxidants & redox signaling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 38 citations in OpenAlex.
- Vitamin E differentially affects short term exercise induced changes in oxidative stress, lipids, and inflammatory markers.Nutrition, metabolism, and cardiovascular diseases : NMCD · 2012Trial
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- Characterization of fecal metabolome changes in patients with obstructive sleep apnea.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2022Article
- Preparation of LDL , Oxidation , Methods of Detection, and Applications in Atherosclerosis Research.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Intestinal and Hepatic Uptake of Dietary Peroxidized Lipids and Their Decomposition Products, and Their Subsequent Effects on Apolipoprotein A1 and Paraoxonase1.Antioxidants (Basel, Switzerland) · 2021Article
- Metabolomic Analysis of Small Extracellular Vesicles Derived from Pancreatic Cancer Cells Cultured under Normoxia and Hypoxia.Metabolites · 2021Article
- Are Fried Foods Unhealthy? The Dietary Peroxidized Fatty Acid, 13-HPODE, Induces Intestinal Inflammation In Vitro and In Vivo.Antioxidants (Basel, Switzerland) · 2020Article
- Azelaic Acid Induces Mitochondrial Biogenesis in Skeletal Muscle by Activation of Olfactory Receptor 544.Frontiers in physiology · 2020Article
- A Novel Mechanism for Atherosclerotic Calcification: Potential Resolution of the Oxidation Paradox.Antioxidants & redox signaling · 2018Article
- Pyruvate enhancement of cardiac performance: Cellular mechanisms and clinical application.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- Differential lipid metabolism in monocytes and macrophages: influence of cholesterol loading.Journal of lipid research · 2016Article
- Sulforaphane attenuates the development of atherosclerosis and improves endothelial dysfunction in hypercholesterolemic rabbits.Experimental biology and medicine (Maywood, N.J.) · 2016Article
- Novel technique for generating macrophage foam cells for in vitro reverse cholesterol transport studies.Journal of lipid research · 2013Article
- Genetic reduction of lipoic acid synthase expression modestly increases atherosclerosis in male, but not in female, apolipoprotein E-deficient mice.Atherosclerosis · 2010Article
- Oxidized LDL: diversity, patterns of recognition, and pathophysiology.Antioxidants & redox signaling · 2010Review
- Anti-atherosclerotic actions of azelaic acid, an end product of linoleic acid peroxidation, in mice.Atherosclerosis · 2010Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The decomposition of peroxidized lipids of low-density lipoprotein (LDL) has been suggested to be involved in atherosclerosis. In this study, an in vitro system with 13-hydroperoxylinoleic acid (13-HPODE) was used to determine the effects of antioxidants on its decomposition. Decomposition of 13-HPODE was not affected by alpha-tocopherol, several other antioxidants, or antioxidant enzymes. Moreover, the inclusion of alpha-tocopherol during the decomposition of 13-HPODE resulted in an accumulation of aldehydes. Further oxidation of aldehydes to carboxylic acids by a number of oxidases was prevented by alpha-tocopherol. Conversely, the formation of carboxylic acids may be conducive to plaque stabilization via immunomodulation, rapid degradation, and by calcium sequestration. Thus, the inhibition of formation of carboxylic acids could be a serious deleterious effect of antioxidant treatment. In contrast, alpha-keto acids, like pyruvic acid, promoted the conversion of 13-HPODE to 13-hydroxylinoleic acid (13-HODE) by readily undergoing decarboxylation into acetate. These observations suggest that agents that promote the reduction of lipid peroxides into lipid hydroxides could be far more effective in treating cardiovascular diseases as opposed alpha-tocopherol-like antioxidants that could affect additional steps in the oxidation cascade.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.