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The effect of lipid peroxidation products on reactive oxygen species formation and nitric oxide production in lipopolysaccharide-stimulated RAW 264.7 macrophages
G. Ambrozova, M. Pekarova, A. Lojek
Language English Country England, Great Britain
Document type Comparative Study, Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Acrolein toxicity MeSH
- Macrophage Activation MeSH
- Aldehydes toxicity MeSH
- Time Factors MeSH
- Down-Regulation drug effects MeSH
- Nitrites metabolism MeSH
- Lipopolysaccharides immunology MeSH
- Macrophages immunology metabolism MeSH
- Malondialdehyde toxicity MeSH
- Mice MeSH
- NADPH Oxidases antagonists & inhibitors MeSH
- Osmolar Concentration MeSH
- Nitric Oxide antagonists & inhibitors metabolism MeSH
- Lipid Peroxidation MeSH
- Reactive Oxygen Species antagonists & inhibitors metabolism MeSH
- Free Radical Scavengers pharmacology MeSH
- Nitric Oxide Synthase Type II metabolism MeSH
- Cell Line, Transformed MeSH
- Cell Survival drug effects MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Comparative Study MeSH
Lipid peroxidation induced by oxidants leads to the formation of highly reactive metabolites. These can affect various immune functions, including reactive oxygen species (ROS) and nitric oxide (NO) production. The aim of the present study was to investigate the effects of lipid peroxidation products (LPPs) - acrolein, 4-hydroxynonenal, and malondialdehyde - on ROS and NO production in RAW 264.7 macrophages and to compare these effects with the cytotoxic properties of LPPs. Macrophages were stimulated with lipopolysaccharide (0.1 μg/ml) and treated with selected LPPs (concentration range: 0.1-100 μM). ATP test, luminol-enhanced chemiluminescence, Griess reaction, Western blotting analysis, amperometric and total peroxyl radical-trapping antioxidant parameter assay were used for determining the LPPs cytotoxicity, ROS and NO production, inducible nitric oxide synthase expression, NO scavenging, and antioxidant properties of LPPs, respectively. Our study shows that the cytotoxic action of acrolein and 4-hydroxynonenal works in a dose- and time-dependent manner. Further, our results imply that acrolein, 4-hydroxynonenal, and malondialdehyde can inhibit, to a different degree, ROS and NO production in stimulated macrophages, partially independently of their toxic effect. Also, changes in enzymatic pathways (especially NADPH-oxidase and nitric oxide synthase inhibition) and NO scavenging properties are included in the downregulation of reactive species formation.
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