scholarly journals Cellular mechanisms of redox cell signalling: role of cysteine modification in controlling antioxidant defences in response to electrophilic lipid oxidation products

2004 ◽  
Vol 378 (2) ◽  
pp. 373-382 ◽  
Author(s):  
Anna-Liisa LEVONEN ◽  
Aimee LANDAR ◽  
Anup RAMACHANDRAN ◽  
Erin K. CEASER ◽  
Dale A. DICKINSON ◽  
...  
Keyword(s):  
Lipid Oxidation ◽  
Molecular Mechanisms ◽  
Intact Cell ◽  
Cell Signalling ◽  
Oxidation Products ◽  
Oxidized Lipids ◽  
Related Factor ◽  
Lipid Oxidation Products ◽  
Electrophilic Lipids ◽  
Prostaglandin J2

The molecular mechanisms through which oxidized lipids and their electrophilic decomposition products mediate redox cell signalling is not well understood and may involve direct modification of signal-transduction proteins or the secondary production of reactive oxygen or nitrogen species in the cell. Critical in the adaptation of cells to oxidative stress, including exposure to subtoxic concentrations of oxidized lipids, is the transcriptional regulation of antioxidant enzymes, many of which are controlled by antioxidant-responsive elements (AREs), also known as electrophile-responsive elements. The central regulator of the ARE response is the transcription factor Nrf2 (NF-E2-related factor 2), which on stimulation dissociates from its cytoplasmic inhibitor Keap1, translocates to the nucleus and transactivates ARE-dependent genes. We hypothesized that electrophilic lipids are capable of activating ARE through thiol modification of Keap1 and we have tested this concept in an intact cell system using induction of glutathione synthesis by the cyclopentenone prostaglandin, 15-deoxy-Δ12,14-prostaglandin J2. On exposure to 15-deoxy-Δ12,14-prostaglandin J2, the dissociation of Nrf2 from Keap1 occurred and this was dependent on the modification of thiols in Keap1. This mechanism appears to encompass other electrophilic lipids, since 15-A2t-isoprostane and the lipid aldehyde 4-hydroxynonenal were also shown to modify Keap1 and activate ARE. We propose that activation of ARE through this mechanism will have a major impact on inflammatory situations such as atherosclerosis, in which both enzymic as well as non-enzymic formation of electrophilic lipid oxidation products are increased.

Cell signalling by oxidized lipids and the role of reactive oxygen species in the endothelium

2005 ◽  
Vol 33 (6) ◽  
pp. 1385-1389 ◽  
Author(s):  
J.W. Zmijewski ◽  
A. Landar ◽  
N. Watanabe ◽  
D.A. Dickinson ◽  
N. Noguchi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Lipid Oxidation ◽  
Protein Function ◽  
Cell Signalling ◽  
Reactive Oxygen ◽  
Oxidation Products ◽  
Oxidized Lipids ◽  
Oxygen Species ◽  
Post Translational Modification ◽  
Lipid Oxidation Products

The controlled formation of ROS (reactive oxygen species) and RNS (reactive nitrogen species) is now known to be critical in cellular redox signalling. As with the more familiar phosphorylation-dependent signal transduction pathways, control of protein function is mediated by the post-translational modification at specific amino acid residues, notably thiols. Two important classes of oxidant-derived signalling molecules are the lipid oxidation products, including those with electrophilic reactive centres, and decomposition products such as lysoPC (lysophosphatidylcholine). The mechanisms can be direct in the case of electrophiles, as they can modify signalling proteins by post-translational modification of thiols. In the case of lysoPC, it appears that secondary generation of ROS/RNS, dependent on intracellular calcium fluxes, can cause the secondary induction of H2O2 in the cell. In either case, the intracellular source of ROS/RNS has not been defined. In this respect, the mitochondrion is particularly interesting since it is now becoming apparent that the formation of superoxide from the respiratory chain can play an important role in cell signalling, and oxidized lipids can stimulate ROS formation from an undefined source. In this short overview, we describe recent experiments that suggest that the cell signalling mediated by lipid oxidation products involves their interaction with mitochondria. The implications of these results for our understanding of adaptation and the response to stress in cardiovascular disease are discussed.

Abstract 421: Aldose Reductase Protects Against the Early Atherosclerotic Lesion Formation InApoe-null Mice

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Sanjay Srivastava ◽  
Oleg Barski ◽  
Aruni Bhatnagar
Keyword(s):  
Lipid Oxidation ◽  
Aldose Reductase ◽  
Atherosclerotic Lesion ◽  
Oxidation Products ◽  
Oxidized Lipids ◽  
Lesion Formation ◽  
Aortic Sinus ◽  
Unsaturated Lipids ◽  
Lipid Oxidation Products ◽  
Atherosclerotic Lesion Formation

Atherosclerotic lesion formation is associated with extensive oxidation of unsaturated lipids and the accumulation of lipid oxidation products. Products of lipid oxidation, particularly aldehydes, stimulate cytokine production and enhance monocyte adhesion. Aldehydes generated by oxidized lipids are metabolized by several biochemical pathways, of which aldose reductase (AR)-catalyzed reduction represents a metabolic fate common to both free and phospholipid esterified aldehydes. Herein, we tested the hypothesis that inhibition of AR could aggravate atherosclerotic lesion formation by preventing the removal and the detoxification of aldehydes generated by oxidized lipids. In atherosclerotic lesions of apoE-null mice, AR protein was associated with macrophage-rich regions and its abundance increased with lesion progression. Treatment of 8 week old apoE-null mice with AR inhibitors sorbinil or tolrestat for 4 weeks increased lesion formation in the aortic arch (P<0.01) and the aortic sinus (P<0.01). No change in lesion formation was observed when 24 week old mice were fed AR inhibitors for 12 weeks. To probe the role of AR in atherogenesis further, we generated AR −/− /apoE −/− mice. Lesions of 8 week old AR −/− /apoE −/− mice maintained on high fat diet for 4 or 12 weeks were significantly larger throughout the aortic tree (P<0.01 for both the groups) when compared with age-matched AR +/+ /apoE −/− mice. Lesions in AR −/− /apoE −/− mice exhibited increased collagen (P<0.01) and macrophage content (P<0.01) and a decrease in smooth muscle cells (P<0.01). GC-MS analysis showed that the concentration of AR substrates HNE and hexanal was increased by 2.5–3 fold (P<0.01) in the plasma of AR −/− /apoE −/− mice as compared with AR +/+ /apoE −/− mice. Immunohistochemical analysis showed greater accumulation of protein-HNE adducts in arterial lesions of AR −/− /apoE −/− mice. These observations suggest that AR is up regulated during atherosclerosis and that this protein protects against early stages of atherosclerotic lesion formation by removing aldehydes generated by lipid oxidation.

Commercial luncheon meat products and their in vitro gastrointestinal digests contain more protein carbonyl compounds but less lipid oxidation products compared to fresh pork

2020 ◽  
Vol 136 ◽  
pp. 109585
Author(s):  
Sophie Goethals ◽  
Thomas Van Hecke ◽  
Els Vossen ◽  
Lynn Vanhaecke ◽  
John Van Camp ◽  
...  
Keyword(s):  
Lipid Oxidation ◽  
Carbonyl Compounds ◽  
Meat Products ◽  
Protein Carbonyl ◽  
Oxidation Products ◽  
Lipid Oxidation Products ◽  
Luncheon Meat ◽  
Protein Carbonyl Compounds

Quercetin Inhibited the Formation of Lipid Oxidation Products in Thermally Treated Soybean Oil by Trapping Intermediates

2021 ◽  
Author(s):  
Xu Zhang ◽  
Ling Ni ◽  
Yamin Zhu ◽  
Ning Liu ◽  
Daming Fan ◽  
...  
Keyword(s):  
Soybean Oil ◽  
Lipid Oxidation ◽  
Oxidation Products ◽  
Lipid Oxidation Products ◽  
Thermally Treated

scholarly journals Determination of lipid oxidation products in vegetable oils and marine omega-3 supplements

2011 ◽  
Vol 55 (1) ◽  
pp. 5792 ◽  
Author(s):  
Bente Lise Halvorsen ◽  
Rune Blomhoff
Keyword(s):  
Lipid Oxidation ◽  
Vegetable Oils ◽  
Oxidation Products ◽  
Omega 3 ◽  
Lipid Oxidation Products

scholarly journals Accumulation of Aluminium and Physiological Status of Tree Foliage in the Vicinity of a Large Aluminium Smelter

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
E. D. Wannaz ◽  
J. H. Rodriguez ◽  
T. Wolfsberger ◽  
H. A. Carreras ◽  
M. L. Pignata ◽  
...  
Keyword(s):  
Lipid Oxidation ◽  
Membrane Lipid ◽  
Physiological Parameters ◽  
Oxidation Products ◽  
Physiological Status ◽  
Pollution Gradient ◽  
Sulphur Deposition ◽  
Aluminium Production ◽  
Lipid Oxidation Products ◽  
Tree Foliage

A pollution gradient was observed in tree foliage sampled in the vicinity of a large aluminium production facility in Patagonia (Argentina). Leaves ofEucalyptus rostrata, and Populus hybridusand different needle ages ofPinusspec. were collected and concentrations of aluminium (Al) and sulphur (S) as well as physiological parameters (chlorophyll and lipid oxidation products) were analyzed. Al and S concentrations indicate a steep pollution gradient in the study showing a relationship with the physiological parameters in particular membrane lipid oxidation products. The present study confirms that aluminium smelting results in high Al and sulphur deposition in the study area, and therefore further studies should be carried out taking into account potentially adverse effects of these compounds on human and ecosystem health.

scholarly journals Feeding Artemisia annua alters digesta pH and muscle lipid oxidation products in broiler chickens

2013 ◽  
Vol 92 (4) ◽  
pp. 1085-1090 ◽  
Author(s):  
G. Cherian ◽  
A. Orr ◽  
I.C. Burke ◽  
W. Pan
Keyword(s):  
Lipid Oxidation ◽  
Broiler Chickens ◽  
Artemisia Annua ◽  
Oxidation Products ◽  
Muscle Lipid ◽  
Lipid Oxidation Products

Volatile Lipid Oxidation Products of Wagyu and Domestic Breeds of Beef

1996 ◽  
Vol 44 (4) ◽  
pp. 1091-1095 ◽  
Author(s):  
Terri D. Boylston ◽  
Sarah A. Morgan ◽  
Kristen A. Johnson ◽  
Ray W. Wright, ◽  
Jan R. Busboom ◽  
...  
Keyword(s):  
Lipid Oxidation ◽  
Oxidation Products ◽  
Lipid Oxidation Products
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