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Lipid Peroxidation

Lipid Peroxidation is the oxidative degradation of lipids, a natural process that occurs in living organisms.
It involves the action of free radicals and reactive oxygen species on lipids, particularly polyunsaturated fatty acids, resulting in cell membrane damage and the production of potentially toxic byproducts.
This process is implicated in the pathogenesis of various diseases, including cardiovascular disorders, neurodegenerative conditions, and cancer.
Understanding the mechanisms and regulation of lipid peroxidation is crucial for developing effective therapies and preventative strategies.
Researchers can optimize their work on this important topic by utilizing the AI-driven platform PubCompare.ai, which helps identify the best protocols, products, and reagents from the scientific literature, preprints, and patents.

Most cited protocols related to «Lipid Peroxidation»

The adult brain slice method we have described has been successfully implemented in a variety of experimental contexts for analysis of diverse brain regions and cell types. However, we would encourage adopters to view this method as a work in progress, and we believe there is still substantial room for systematic improvement. As a case in point, we have observed that mature adult brain slices experience high levels of oxidative stress due in large part to rapid depletion of cellular antioxidants including ascorbate and reduced glutathione (GSH). This can lead to lipid peroxidation, neuronal membrane rigidity, and tissue deterioration. There appears to be a nonuniform susceptibility to this form of oxidative damage, for example, CA1 and CA3 pyramidal neurons are particularly vulnerable, making patch clamp recording of these cells difficult in brain slices from adult and aging animals in spite of the protective recovery method.
The specific restoration of intracellular pools of neuronal GSH (e.g. supplementation with the cell-permeable GSH-ethyl ester) is highly effective at curbing deterioration and prolonging slice viability under these circumstances. Thus, we have been able to further improve the NMDG recovery method by devising strategies for stimulating de novo synthesis of glutathione during acute brain slice preparation and incubation. This is most readily accomplished by adding the inexpensive GSH precursor N-acetyl-L-cysteine (NAC, 5–12 mM) to the NMDG aCSF and HEPES holding aCSF formulas, but not the recording aCSF (seeNote 14). NAC is cell-permeable and has been shown to specifically increase neuronal glutathione levels in brain tissue (26 (link)). Within 1–2 hours of slice preparation we are able to observe notable improvements in the general appearance of neurons and in the ease of patch clamp recording, and the slices are able to be maintained in a healthy state for extended time periods.
Although these more advanced methods are not absolutely required for successful adult brain slice patch clamp recordings (as demonstrated by the specific application we have described in this chapter), we include this information in hopes of providing more options to extend the versatility of our method for particularly challenging applications. Glutathione restoration is highly effective at maintaining healthy brain slices but may not be appropriate in every experimental context, e.g. investigations focusing on oxidative stress in the aging brain. On the other hand, without implementing the NMDG protective recovery method together with glutathione restoration strategy, targeted patch clamp analysis in brain slices from very old animals is prohibitively challenging.
Publication 2014
Acetylcysteine Adult Anabolism Animals Antioxidants Brain Cells Diet, Formula Esters Gastrin-Secreting Cells Glutathione HEPES Lipid Peroxidation Muscle Rigidity Neurons Oxidative Damage Oxidative Stress Permeability Protoplasm Pyramidal Cells Reduced Glutathione Susceptibility, Disease Tissue, Membrane Tissues
All animal procedures were approved by the Animal Care and Use Committee of Zhejiang University. The generation of Ripk3−/−, Mlkl−/−, Fadd−/−Mlkl−/−, and Nrf2−/− mice (17 (link), 49 (link), 50 (link)), LC/MS analysis, iron assay, and methods used in surgery, drug treatment, cell culture, histology, lipid peroxidation detection, and mitochondria isolation are provided in SI Appendix, SI Materials and Methods. Except where indicated otherwise, all summary data are presented as the mean ± SEM. The Student’s t test was used to compare two groups, and the log-rank test was used to analyze the survival curves. Differences with a P value of <0.05 were considered statistically significant.
Publication 2019
Animals Biological Assay Cell Culture Techniques FADD protein, human Iron isolation Lipid Peroxidation Mice, House Mitochondria NFE2L2 protein, human Operative Surgical Procedures Pharmaceutical Preparations RIPK3 protein, human Student
The activity for SOD in sera and brains was examined according to xanthine oxidase method provided by the standard assay kit (Nanjing Jiancheng Bioengineering Institute, China) as described [17 (link)]. The assay used the xanthine-xanthine oxidase system to produce superoxide ions, which reacted with 2-(4-iodophenyl)-3-(4-nitrophenol-5-phenlyltetrazolium chloride) to form a red formazan dye, and the absorbance at 550 nm was determined. The values were expressed as units per mg protein, and protein concentration was determined by a BCA protein assay kit (Pierce Chemical Co.), where one unit of SOD was defined as the amount of SOD inhibiting the rate of reaction by 50% at 25°C.
Lipid peroxidation was evaluated by measuring MDA concentrations according to the thiobarbituric acid (TBA) method as commercially recommended (Nanjing Jiancheng Bioengineering Institute, China). The method was based on the spectrophotometric measurement of the color produced during the reaction to TBA with MDA. MDA concentrations were calculated by the absorbance of TBA reactive substances (TBARS) at 532 nm.
Publication 2012
4-nitrophenol Biological Assay Brain Chlorides Formazans Ions Lipid Peroxidation Proteins Serum Spectrophotometry Staphylococcal Protein A Superoxides thiobarbituric acid Thiobarbituric Acid Reactive Substances Xanthine Oxidase
Oxidative modifications products were assessed both in the plasma and tissue homogenates.
Advanced Oxidation Protein Products (AOPP) were estimated colorimetrically using a method Kalousová et al. (2002 (link)), which measures the total iodide ion oxidizing capacity of the samples. Absorbance at 340 nm was measured immediately by Infinite M200 PRO Multimode Microplate Reader, Tecan.
Advanced glycation end products (AGE) were estimated spectrofluorimetrically at the excitation and emission wavelengths of 350 and 440 nm using Infinite M200 PRO Multimode Microplate Reader, Tecan. Results were expressed as fluorescence/mg of the total protein.
The content of dityrosine, kynurenine, N-formylkynurenine and tryptophan was analyzed spectrofluorimetrically on 96-well microplates measuring the characteristic fluorescence at 330/415, 365/480, 325/434, and 95/340 nm respectively by Infinite M200 PRO Multimode Microplate Reader, Tecan. Results were expressed as fluorescence/mg of the total protein.
Lipid peroxidation was estimated colorimetrically using the Thiobarbituric Acid Reactive Substances (TBARS) method for measuring a malondialdehyde (MDA). 1,3,3,3 tetraethoxypropane was used as a standard (Buege and Aust, 1978 (link)).
The concentration of 4-hydroxynonenal (4-HNE) protein adducts was measured by commercial enzyme-linked immunosorbent assay (ELISA) according to the manufacturer's instructions (OxiSelect™ HNE Adduct Competitive ELISA Kit, Cell Biolabs, Inc. San Diego, CA, USA). The quantity of 4-HNE protein adducts was determined colorimetrically from a calibration curve for 4-HNE-BSA.
Total oxidant status (TOS) was measured colorimetrically based on the oxidation of ferrous ion (Fe2+) to ferric ion (Fe3+) in the presence of oxidants comprised in a sample (Erel, 2005 (link)). Changes in absorbance of the reaction solution were measured bichromatically (560/800 nm) in triplicate samples. The results were expressed as micromolar hydrogen peroxide (H2O2) equivalent per mg of the total protein (μmol H2O2 Equiv/mg of the total protein).
Oxidative stress index (OSI) was calculated according to the formula: OSI = TOS/TAC·100% (Knaś et al., 2016 (link)).
The total protein content was determined colorimetrically using the bicinchoninic acid assay (BCA assay) with bovine serum albumin (BSA) as a standard (Thermo Scientific PIERCE BCA Protein Assay Kit, Rockford, IL, USA).
All assays were performed in duplicate samples, except for the TOS determination (see above) and converted to mg of the total protein. Graphical representation of the experiment was presented on Figure 1.
Publication 2017
Advanced Oxidation Protein Products bicinchoninic acid Biological Assay Cells dityrosine Enzyme-Linked Immunosorbent Assay Fluorescence Glycation End Products, Advanced Iodides Kynurenine Lipid Peroxidation M-200 Malondialdehyde N'-formylkynurenine Oxidants Oxidative Stress Peroxide, Hydrogen Plasma Proteins Serum Albumin, Bovine Thiobarbituric Acid Reactive Substances Tissues Tryptophan
Thiobarbituric acid (TBA) test is a commonly used method to determine lipid peroxidation. This method is based on the reaction of TBA with malondialdehyde (MDA), one of the aldehyde products of lipid peroxidation. The sample is heated with TBA under acidic conditions; MDA forms an adduct with TBA and produces a pink colored product, which is measured spectrophotometrically at 532 nm (16 (link)). There is considerable controversy regarding the specificity of TBA for MDA because several other substances in tissues and body fluids can also react nonspecifically with TBA producing a chromogen with absorbance between 530 to 535 nm. However, MDA has been shown to be a predominant product when cellular organelles are subjected to peroxidation in vitro. Hence TBA assay has been extensively used for studies on lipid peroxidation in vitro.
Publication 2010
Acids Aldehydes azo rubin S Biological Assay Body Fluids Lipid Peroxidation Malondialdehyde Organelles thiobarbituric acid Tissues

Most recents protocols related to «Lipid Peroxidation»

In plasma samples, the following oxidative stress markers were measured: nitrite (NO2), superoxide anion radical (O2), hydrogen peroxide (H2O2), and the index of lipid peroxidation (measured as TBARS – thiobarbituric acid reactive substances).
Nitric oxide decomposes rapidly to form stable metabolite nitrite/nitrate products. The nitrite level was measured and used as an index of nitric oxide (NO) production using the Griess reagent. A total of 0.5 ml of plasma was precipitated with 200 μl of 30% sulphosalicylic acid, vortexed for 30 min, and centrifuged at 3000 × g. Equal volumes of supernatant and Griess reagent containing 1% sulphanilamide in 5% phosphoric acid/0.1% naphthalene ethylenediamine dihydrochloride were added and incubated for 10 min in the dark, and the sample was measured at 543 nm. The nitrite levels were calculated using sodium nitrite as the standard [13 (link)].
The O2 concentration was measured after the reaction of nitro blue tetrazolium in Tris buffer with the plasma at 530 nm. Distilled water served as the blank [14 ].
The measurement of H2O2 is based on the oxidation of phenol red by H2O2 in a reaction catalysed by horseradish peroxidase (HRPO). Two hundred μl of plasma was precipitated with 800 ml of freshly prepared phenol red solution, followed by the addition of 10 μl of (1:20) HRPO (made ex tempore). Distilled water was used as the blank instead of the plasma sample. H2O2 was measured at 610 nm [15 (link)].
The degree of lipid peroxidation in the plasma samples was estimated by measuring TBARS using 1% thiobarbituric acid in 0.05 NaOH, incubated with the plasma at 100 °C for 15 min, and measured at 530 nm. Distilled water served as the blank [16 (link)].
The activity of the following antioxidants in the lysate was determined: reduced glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). The level of reduced glutathione was determined based on GSH oxidation with 5,5-dithiobis-6,2-nitrobenzoic acid using a method by Beutler [17 ]. The CAT activity was determined according to Aebi [18 (link)]. The lysates were diluted with distilled water (1:7 v/v) and treated with chloroform-ethanol (0.6:1 v/v) to remove haemoglobin, and then 50 μl of CAT buffer, 100 μl of sample and 1 ml of 10 mM H2O2 were added to the samples. The detection was performed at 360 nm. SOD activity was determined by the epinephrine method of Beutler [19 (link)]. Lysate (100 μl) and 1 ml carbonate buffer were mixed, and then 100 μl of epinephrine was added. The detection was performed at 470 nm.
Publication 2023
Anions Antioxidant Activity Buffers Carbonates Catalase Chloroform Epinephrine Ethanol ethylenediamine dihydrochloride Griess reagent Hemoglobin Horseradish Peroxidase Lipid Peroxidation naphthalene Nitrates Nitrites Nitrobenzoic Acids Nitroblue Tetrazolium Oxidative Stress Oxide, Nitric Peroxide, Hydrogen Phosphoric Acids Plasma Reduced Glutathione Sodium Nitrite Sulfanilamide sulfosalicylic acid Superoxide Dismutase Superoxides thiobarbituric acid Thiobarbituric Acid Reactive Substances Tromethamine
At 9.5 weeks old, the mice were anesthetized, and their blood samples were collected by cardiac puncture and placed in EDTA containing tubes. The animals were sacrificed under anesthesia with 1% ketamine. and their spleens were excised and weighed. A portion of the spleen was washed with the washing buffer and homogenized, and the supernatant obtained was used for lipid peroxidation assay. A portion of the splenic tissue was fixed in 10% formalin solution and stored for histological analysis.
Publication 2023
Anesthesia Animals Biological Assay BLOOD Buffers Edetic Acid Formalin Heart Ketamine Lipid Peroxidation Mice, House Punctures Spleen
The chlorophyll quantification was done by using spectrophotometry, by following the method described by Arnon (1949) (link). The lipid peroxidation end products were measured by determining the amount of TBARS using the TBA reaction method described by Heath and Packer (1968) (link).
Publication 2023
Chlorophyll Lipid Peroxidation Spectrophotometry Thiobarbituric Acid Reactive Substances
A selection of
sublethal end points related to, e.g., neurological impacts, lipid
metabolism, and oxidative responses of shrimp were addressed in the
study. Validated protocols were used to analyze the following parameters:
acetylcholinesterase activity (AChE) in gills and muscle tissues to
assess neurotoxicity; AcylCoA (acyl coenzyme A) oxidase activity (ACOX),
involved in different aspects of lipid homeostasis in the digestive
gland; antioxidant response and oxidative damage in digestive gland
by total oxyradical scavenging capacity (TOSC assay toward peroxyl
and hydroxyl radicals); and lipid peroxidation (malondialdehyde levels).
The parameters described above were analyzed in tissues at the end
of exposure (day 4) and at the end of the recovery period (day 14).
Analytical methods are described in the SI.
Publication 2023
Acetylcholinesterase Acyl CoA Oxidase Acyl Coenzyme A Antioxidants Biological Assay Digestive System Gills Homeostasis Hydroxyl Radical Lipid Peroxidation Lipids Malondialdehyde Muscle Tissue Neurotoxicity Syndromes Oxidative Damage Pain Tissues
Glucose (enzymatic-colorimetric method, sensitivity: 0.06 mmol/L) and urea (kinetic method, sensitivity: 0.056 mmol/L) concentrations were determined in plasma with an automatic analyzer (Gernon, RAL S.A, Barcelona, Spain). The mean intra- and interassay CV were 1.5% and 1.9% for glucose and 3.2% and 4.8% for urea, respectively. Plasma BHB (kinetic enzymatic method, sensitivity: 0.100 mmol/L) and NEFA (colorimetric method, sensitivity: 0.072 mmol/L) were determined using Randox kits (Randox Laboratories Ltd., Country Antrim, UK). The mean intra- and interassay CV were respectively 3.3% and 3.7% for NEFA and 6.2% in both cases for BHB. Oxidative status was determined using MDA as a biomarker of lipid peroxidation. This indicator was determined by liquid chromatography using an Acquity UPLC H-Class liquid chromatograph (Waters, Milford, MA, USA) equipped with a silica-based bonded phase column (Acquity UPLC HSS PFP, 100 mm × 2.1 mm × 1.8 μm, Waters), an absorbance detector (Acquity UPLC Photodiode Array PDA eλ detector, Waters) and a fluorescence detector (2475 Multi λ Fluorescence Detector, Waters). The quantification of MDA was done by fluorescence detection at ʎexcitation = 530 nm and ʎemission = 550 nm following the chromatographic conditions described in Bertolín et al. (2019) (link). The mean intra- and interassay CV were 4.6% and 7.3%, respectively.
Publication 2023
Biological Markers Chromatography Colorimetry Enzymes Fluorescence Glucose Hypersensitivity Kinetics Lipid A Lipid Peroxidation Liquid Chromatography Nonesterified Fatty Acids Plasma Randox Silicon Dioxide Urea

Top products related to «Lipid Peroxidation»

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The Lipid Peroxidation MDA Assay Kit is a laboratory tool designed to measure the levels of malondialdehyde (MDA), a marker of lipid peroxidation. The kit provides a colorimetric method to quantify MDA concentrations in various biological samples.
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The TBARS assay kit is a laboratory tool used to measure the levels of thiobarbituric acid reactive substances (TBARS) in biological samples. TBARS are commonly used as a biomarker for oxidative stress and lipid peroxidation. The kit provides the necessary reagents and protocols to perform this analysis.
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BODIPY 581/591 C11 is a fluorescent lipid probe used for the detection and quantification of lipid peroxidation in biological samples. It exhibits a shift in fluorescence emission from red to green upon oxidation, allowing for the monitoring of oxidative processes.
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The Lipid Peroxidation Assay Kit is a laboratory equipment designed to measure the levels of lipid peroxidation in biological samples. It provides a quantitative assessment of malondialdehyde (MDA), a marker of oxidative stress and lipid damage.
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Ab118970 is a lab equipment product from Abcam. It is a recombinant protein that can be used in various research applications. The core function of this product is to provide a standardized and reliable reagent for scientific experiments.
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The MDA Assay Kit is a colorimetric assay designed to quantify malondialdehyde (MDA), a marker of oxidative stress. The kit uses a thiobarbituric acid reaction to detect MDA levels in various sample types, including tissues, cells, and biological fluids.
Sourced in United States, Germany, Sao Tome and Principe
The Lipid Peroxidation (MDA) Assay Kit is a laboratory tool used to measure the level of malondialdehyde (MDA), a byproduct of lipid peroxidation. It provides a quantitative assessment of oxidative stress in biological samples.
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The Lipid Peroxidation (MDA) Assay Kit is a laboratory tool designed to measure the level of malondialdehyde (MDA), a byproduct of lipid peroxidation. This assay provides a quantitative analysis of MDA concentration in biological samples.
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The MDA assay kit is a laboratory tool used to quantify the levels of malondialdehyde (MDA), a biomarker for oxidative stress. The kit provides reagents and protocols for a colorimetric or fluorometric assay to measure MDA concentrations in various biological samples, such as cell lysates, tissue homogenates, or biological fluids.
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Thiobarbituric acid is a chemical compound used in various laboratory applications. It is a white to pale yellow crystalline solid that is soluble in water and organic solvents. Thiobarbituric acid is commonly used as a reagent in analytical techniques to detect the presence of certain compounds, particularly those related to lipid peroxidation.

More about "Lipid Peroxidation"

Lipid peroxidation is a natural biological process involving the oxidative degradation of lipids, particularly polyunsaturated fatty acids, by free radicals and reactive oxygen species.
This process can lead to cell membrane damage and the production of potentially toxic byproducts, such as malondialdehyde (MDA).
Lipid peroxidation has been implicated in the pathogenesis of various diseases, including cardiovascular disorders, neurodegenerative conditions, and cancer.
Understanding the mechanisms and regulation of lipid peroxidation is crucial for developing effective therapies and preventative strategies.
Researchers can utilize specialized assays and kits, such as the TBARS assay, BODIPY 581/591 C11, and Lipid Peroxidation Assay Kit, to measure and quantify lipid peroxidation levels.
These tools can help identify the most effective protocols, products, and reagents for studying this important biological process.
By leveraging the AI-driven platform PubCompare.ai, researchers can optimize their work on lipid peroxidation by accessing the latest scientific literature, preprints, and patents.
This platform allows users to compare and identify the best methods, products, and reagents, helping to elevate the reproducibility and effectiveness of their research.
With PubCompare.ai, the future of reproducible research on lipid peroxidation is here.