1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphorylcholine and 4-hydroxy-2-nonenal

1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphorylcholine has been researched along with 4-hydroxy-2-nonenal* in 3 studies

Other Studies

3 other study(ies) available for 1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphorylcholine and 4-hydroxy-2-nonenal

ArticleYear
Lipid peroxidation increases hydrogen peroxide permeability leading to cell death in cancer cell lines that lack mtDNA.
    Cancer science, 2019, Volume: 110, Issue:9

    4-Hydroxynonenal (HNE) is an important product of plasma membrane lipid peroxidation, which is a cause of cell and tissue injury. Mitochondrial DNA (mtDNA)-depleted ρ

    Topics: Aldehydes; Apoptosis; Arachidonate 15-Lipoxygenase; Cell Line, Tumor; Cell Membrane; Cell Membrane Permeability; DNA, Mitochondrial; Drug Resistance, Neoplasm; Electron Transport Chain Complex Proteins; Humans; Hydrogen Peroxide; Lipid Peroxidation; Mitochondria; Neoplasms; Oxidative Stress; Phospholipid Ethers; Up-Regulation

2019
Rapid formation of 4-hydroxy-2-nonenal, malondialdehyde, and phosphatidylcholine aldehyde from phospholipid hydroperoxide by hemoproteins.
    Free radical biology & medicine, 2004, Apr-15, Volume: 36, Issue:8

    4-Hydroxy-2-nonenal (HNE) and malondialdehyde (MDA) are well-known toxic products of lipid peroxidation. Phosphatidylcholine aldehydes are also known as oxidation products of phosphatidylcholine. The mechanism of the formation of these compounds in vivo has been a long-standing question. We observed that the rapid reaction of hemoproteins (methemoglobin, metmyoglobin, and cytochrome c) with 1-palmitoyl-2-(13-hydroperoxy-cis-9, trans-11-octadecadienoyl) phosphatidylcholine (PLPC-OOH), having a hydroperoxylinoleoyl residue, generated HNE, MDA, and the phosphatidylcholine aldehyde 1-palmitoyl-2-(9-oxononanoyl) phosphatidylcholine. The efficiencies (mol% yield) of the formation of HNE and MDA from decomposed PLPC-OOH by methemoglobin, metmyoglobin, and cytochrome c after incubation for 10 min were 1.6, 1.0, and 1.0% for HNE and 1.2, 0.6, and 0.9% for MDA, respectively. When 1-palmitoyl-2-linoleoyl phosphatidylcholine was incubated with lipoxidase and methemoglobin, the formation of HNE and the phosphatidylcholine aldehyde 1-palmitoyl-2-(9-oxononanoyl) phosphatidylcholine was observed. When 1-palmitoyl-2-arachidonyl phosphatidylcholine was used instead of 1-palmitoyl-2-linoleoyl phosphatidylcholine, the phosphatidylcholine aldehyde 1-palmitoyl-2-oxovaleroyl phosphatidylcholine was obtained. These data suggest that HNE and phosphatidylcholine aldehydes might be rapidly formed from phosphatidylcholine by lipoxygenase and hemoproteins. Furthermore, hemichrome, converted from methemoglobin by deoxycholic acid and ursodeoxycholic acid, showed marked decomposition of HNE. These results suggest that hemoproteins are related to both the formation and the decomposition of HNE.

    Topics: Aldehydes; Antioxidants; Deoxycholic Acid; Free Radicals; Hemeproteins; Hemoglobins; Hydrogen Peroxide; Lipid Metabolism; Lipid Peroxidation; Lipoproteins; Lipoxygenase; Malondialdehyde; Methemoglobin; Models, Chemical; Phosphatidylcholines; Phospholipid Ethers; Time Factors; Ultraviolet Rays; Ursodeoxycholic Acid

2004
Involvement of aldose reductase in the metabolism of atherogenic aldehydes.
    Chemico-biological interactions, 2001, Jan-30, Volume: 130-132, Issue:1-3

    Phospholipid peroxidation generates a variety of aldehydes, which includes free saturated and unsaturated aldehydes, and aldehydes that remain esterified to the phosphoglyceride backbone - the so-called 'core' aldehydes. However, little is known in regarding the vascular metabolism of these aldehydes. To identify biochemical pathways that metabolize free aldehydes, we examined the metabolism of 4-hydroxy-trans-2-nonenal in human aortic endothelial cells. Incubation of these cells with [3H]-HNE led to the generation of four main metabolites, i.e. glutathionyl HNE (GS-HNE), glutathionyl dihydroxynonene (GS-DHN), DHN and 4-hydroxynonanoic acid (HNA), which accounted for 5, 50, 6, and 23% of the total HNE metabolized. The conversion of GS-HNE to GS-DHN was inhibited by tolrestat, indicating that it is catalyzed by aldose reductase (AR). The AR was also found to be an efficient catalyst for the reduction of the core aldehyde - 1-palmitoyl-2- (5-oxovaleroyl)-sn-glycero-3-phosphorylcholine, which is generated in minimally modified low-density lipoprotein, and activates the endothelium to bind monocytes. As determined by electrospray mass spectrometry, reduction of POVPC (m/z=594) by AR led to the formation of 1-palmitoyl-2- (5)-hydrovaleryl-sn-glycero-3-phosphorylcholine (PHVPC; m/z=596). These observations suggest that due to its ability to catalyze the reduction of lipid-derived aldehydes AR may be involved in preventing inflammation and diminishing oxidative stress during the early phases of atherogenesis.

    Topics: Aldehyde Reductase; Aldehydes; Arteriosclerosis; Cells, Cultured; Endothelium, Vascular; Glutathione; Humans; Lipoproteins, LDL; Oxidation-Reduction; Phospholipid Ethers

2001