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Oxidative Stress

Oxidative stress is a state of imbalance between the production of free radicals and the body's ability to detoxify them.
This condition can lead to cellular damage and has been implicated in a wide range of diseases, including cardiovascular disorders, neurodegenerative conditions, and cancer.
Optimizing research in this area is crucial for developing effective therapies and preventive strategies.
PubCompare.ai's AI-driven platform can help researchers easily locate relevant protocols from literature, pre-prints, and patents, then use intelligent comparisons to identify the best methods and products.
This innovative solution can enhance the reproducibility and accuracy of oxidative stress studies, empowering researchers to discover the power of AI-fueled research optimization.

Most cited protocols related to «Oxidative Stress»

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
The overall objective of this study was to conduct a longitudinal assessment of the association of endogenous hormones with biomarkers of oxidative stress and antioxidant status during the menstrual cycle. There were four main objectives. The first was to study the intra-menstrual cycle variation of various measures of oxidative stress. This objective is intended to assess variation in several measures of oxidative stress during different phases of the menstrual cycle, including F2-8-isoprostanes in serum. Assessment of variation across individuals is planned. The second objective was to determine the relationship between specific reproductive hormone levels and oxidative stress during specific times in the menstrual cycle of premenopausal women. The panel of reproductive hormones in the blood that were of primary interest are oestradiol, progesterone, LH, FSH and sex hormone binding globulin (SHBG). The third objective was to examine the influence of external factors on both oxidative stress and hormone levels, and their interrelation. The study measured various biological factors that might influence oxidative stress, including serum concentration of certain antioxidant vitamin levels (retinoids, tocopherols, carotenoids and ascorbic acid). In addition, the study assessed other factors that might affect oxidative stress such as medication and supplement intake, cigarette smoking, alcohol consumption, dietary intake, physical activity and levels of stress. Lastly, the study was designed to evaluate the validity and reproducibility of the various biological markers included in the BioCycle study.
Publication 2009
Antioxidants Ascorbic Acid Biological Factors Biological Markers BLOOD Carotenoids Dietary Supplements Estradiol F2-Isoprostanes Hormones Menstrual Cycle Oxidative Stress Pharmaceutical Preparations Progesterone Reproduction Retinoids Serum Sex Hormone-Binding Globulin Tocopherol Vitamins Woman
To determine the carbon, nitrogen, phosphorus and sulfur sources that could support simulated growth, we screened all of the metabolites that could be exchanged with the environment (i.e., exchange reactions) in the iAF1260 and iJR904 models. The identified metabolites formed the potential substrate sets (Table IV). Through subsequent simulations, we set an arbitrary maximum flux of 20 mmol substrate gDW−1 h−1 for each potential substrate tested (consistent with maximum observed substrate uptake rates in vivo) and optimized for flux through the BOFCORE using FBA and either iAF1260 or iJR904. An OUR of 18.5 mmol gDW−1 h−1, the BOFCORE, a NGAM of 8.39 mmol ATP gDW−1 h−1, a GAM of 59.81 mmol ATP gDW−1 and no regulatory constrains were used during the growth condition analysis of iAF1260 (for iJR904, see Reed et al, 2003 (link)). During the analysis, the reactions CAT, SPODM and SPODMpp were constrained to zero to prevent generation of cellular energy equivalents through reactions involved in E. coli's response to oxidative stress. If a positive flux could be generated through the BOFCORE reaction (vBOFcore>0), then the substrate was considered a viable source. Experimental data used in the comparison were provided by Biolog (http://www.biolog.com) and both ‘weak' and ‘positive' readings from the biolog data were considered as a positive growth condition.
Publication 2007
Carbon Cells Debility Growth Disorders Nitrogen Oxidative Stress Phosphorus Sulfur
The primary objectives of the CNSR-III were to establish Chinese ischaemic cerebrovascular disease aetiology classification cohort based on standard diagnosis procedures, identify imaging and biological markers for prognosis of the patients with ischaemic stroke and further establish the predictive model of stroke recurrence based on imaging and biological markers in ischaemic cerebrovascular diseases. The secondary objectives included evaluation of the association of chronic kidney disease (CKD), abnormal glucose regulation, oxidative stress, homocysteine, intestinal flora, heart rate variability and outcome of ischaemic cerebrovascular diseases and its subtypes.
Publication 2019
Biological Markers Cerebrovascular Accident Cerebrovascular Disorders Chinese Chronic Kidney Diseases Glucose Homocysteine Intestinal Microbiome Oxidative Stress Patients Prognosis Rate, Heart Recurrence Stroke, Ischemic Tests, Diagnostic
All animals were treated in accordance with the Guide for the Care and Use of Laboratory Animals as adopted by the U.S. National Institutes of Health and approval was granted by the Ethics Committee of the University Medical Center Mainz and the Landesuntersuchungsamt Rheinland-Pfalz (Koblenz, Germany; permit number: 23 177-07/G 12-1-021 E3 and 23 177-07/G 15-1-094). Noise exposure consisted of repetitive playbacks of a 2 hour long noise pattern of 69 aircraft noise events with a duration of 43 s and a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A), which does not lead to hearing loss.24 (link) Noise events were separated by silent periods with irregular distribution to prevent early adaptation. The noise pattern was played back from downward facing loudspeakers mounted approximately 30 cm above the mouse cages with a Grundig MS 540 compact sound system with a total output of 65 W. Loudness and corresponding sound pressure levels were calibrated with a Class II Sound level meter (Casella CEL-246) within one the cages at initial setup. Actual SPLs during exposure was continuously recorded during the study period with the same device placed between cages with upward facing microphone. The average SPL (Leq3) is 72 dB(A) at a usual background noise level of 48 dB(A) in the animal facility. In control experiments, mice were exposed to ‘white noise’ (this is a random noise with constant spectral density within the range of human hearing from 20 Hz to 20 kHz) using exactly the same average SPL as for aircraft noise. All SPL and maximum sound pressure levels were measured within the mouse cages.
For further information of the methodology employed for determination of blood pressure, stress hormones, vascular function, nitric oxide quantification, oxidative stress parameters, inflammatory pathways, gene and protein expression, next generation sequencing see the Supplementary material online.
Publication 2017
Acclimatization Animals Animals, Laboratory Blood Physiological Phenomena Determination, Blood Pressure Ethics Committees Genes Hearing Impairment Homo sapiens Hormones Inflammation Medical Devices Mus Oxidative Stress Oxide, Nitric Pressure Proteins Sound

Most recents protocols related to «Oxidative Stress»

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Example 5

Human brain astrocytes play a key role in maintaining nerve cell function and survival against oxidative stress. Exposure of cultured human brain astrocytes to H2O2 causes significant damages to the cells, and caused them to release large amounts of LDH. However, pretreatment of the brain cells with Xe-ELIP reagents markedly reduced LDH release (FIG. 15), indicating a protective effect of Xe-ELIP on the brain cells injured by the oxidative stress. No or little protective effect was found in the cells treated with ELIP alone or control media (FIG. 15).

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Patent 2024
Astrocytes Brain Cells Cytotoxin Homo sapiens Neurons Oxidative Stress Peroxide, Hydrogen

Example 4

FIG. 6—(A) VLC-PUFA and elovanoids ELV1 and ELV2 mediated effect on Bid upregulation in ARPE-19 cells under stress. This figure displays the downregulation of the proapoptotic protein of the Bcl2 family Bid by western blot analysis by VLC-PUFA and elovanoids in RPE cells in culture under oxidative-stress. Results indicate that upregulated Bid protein by OS, as evident from the figure, was inhibited by both elovanoids and VLC-PUFA. It is interesting to see that the sodium salts of the elovaniod precursors are more effective than the methyl ester forms. (B) VLC-PUFA and ELV1 and ELV2 compounds mediated upregulation of Bid in ARPE-19 cells under stress. This Figure shows the quantification of Bid downregulation.

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Patent 2024
Apoptosis Inducing Proteins bcl-2 Gene Bid Protein Cells Down-Regulation Esters Inflammation Neurodegenerative Disorders Oxidative Stress Polyunsaturated Fatty Acids Salts Sodium Therapeutics Up-Regulation (Physiology) Western Blot
Not available on PMC !

Example 8

FIG. 10—(A) Effect of NPD1 and VLC-PUFA C32:6 and C34:6 in mediating upregulation of SIRT1 in ARPE-19 cells. (B) Quantification of SIRT1 upregulation by NPD1, C32:6 and C34:6. SIRT1 (Sirtuin1) belongs to a family of highly conserved proteins linked to caloric restriction beneficial outcomes and aging by regulating energy metabolism, genomic stability and stress resistance. SIRT1 is a potential therapeutic target in several diseases including cancer, diabetes, inflammatory disorders, and neurodegenerative diseases or disorders. Elovanoids induce cell survival involving the upregulation of the Bcl2 class of survival proteins and the downregulation of pro-apoptotic Bad and Bax under oxidative stress (OS) in RPE cells. The data in this Figure suggest that elovanoids upregulate SIRT1 abundance in human RPE cells when confronted with OS. As a consequence, remarkable cell survival takes place. This target of elovanoids might be relevant to counteract consequences of several diseases associated with SIRT1.

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Patent 2024
Anastasis B-Cell Leukemia 2 Family Proteins Caloric Restriction Cells Cell Survival Diabetes Mellitus Energy Metabolism Genomic Stability Homo sapiens Inflammation Malignant Neoplasms Neurodegenerative Disorders Oxidative Stress Polyunsaturated Fatty Acids Sirtuin 1 Staphylococcal Protein A Therapeutics Up-Regulation (Physiology)
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Example 4

At 4 weeks after PNx surgery, a significant activation of c-Src (FIG. 5D, p<0.01 vs Sham) and ERK1/2 (FIG. 5E, p<0.01 vs Sham) was observed in LV homogenates in PNx group that was attenuated in those PNx animals given CoPP or pNaKtide (both p<0.01 vs PNx). Comparing to sham group, PNx stimulated protein carbonylation, an oxidative stress marker, in LV homogenates (FIGS. 6A-6B, p<0.01 vs Sham). Administration of CoPP and pNaKtide reduced PNx-induced protein carbonylation (FIGS. 6A-6B, both p<0.01 vs PNx). TBARS data were consistent with the carbonylation data as expected (FIG. 7).

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Patent 2024
Animals COPP protocol Heart Mitogen-Activated Protein Kinase 3 Operative Surgical Procedures Oxidants Oxidative Stress pNaKtide Protein Carbonylation Thiobarbituric Acid Reactive Substances
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.
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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

Top products related to «Oxidative Stress»

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CM-H2DCFDA is a fluorogenic dye that measures hydroxyl, peroxyl, and other reactive oxygen species (ROS) activity in cells. It is a cell-permeable indicator for ROS that is non-fluorescent until the acetate groups are removed by intracellular esterases and oxidation occurs within the cell.
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Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
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The Muse Oxidative Stress Kit is a lab equipment product designed to measure oxidative stress in biological samples. It provides quantitative analysis of oxidized proteins, a key indicator of oxidative stress levels.
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The Muse Cell Analyzer is a compact, fully automated cell analysis system designed for sample preparation and high-throughput analysis. The instrument utilizes the principles of flow cytometry to provide accurate and reliable cell counts, viability, and cell population analysis.
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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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The CellROX Green Reagent is a fluorescent dye used to detect reactive oxygen species (ROS) in live cells. It is a cell-permeant dye that exhibits green fluorescence upon oxidation by ROS, providing a quantitative measure of oxidative stress within the cell.
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Paraquat is a chemical compound used as a laboratory reagent. It is a highly effective herbicide and desiccant. Paraquat is commonly used in research and analytical applications that require a potent oxidizing agent.
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The RT2 First Strand Kit is a laboratory reagent used for the reverse transcription of RNA to cDNA. It provides the necessary components for the conversion of RNA to cDNA, which is a crucial step in various molecular biology applications, such as gene expression analysis and real-time PCR.
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DCFH-DA is a fluorogenic probe used for the detection of reactive oxygen species (ROS) in biological systems. It is a cell-permeable compound that undergoes oxidation in the presence of ROS, resulting in the formation of the highly fluorescent compound 2',7'-dichlorofluorescein (DCF). The intensity of the fluorescence signal is proportional to the level of ROS present in the sample, making DCFH-DA a useful tool for studying oxidative stress and cellular redox status.
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The RNeasy Mini Kit is a laboratory equipment designed for the purification of total RNA from a variety of sample types, including animal cells, tissues, and other biological materials. The kit utilizes a silica-based membrane technology to selectively bind and isolate RNA molecules, allowing for efficient extraction and recovery of high-quality RNA.

More about "Oxidative Stress"

Oxidative stress is a state of imbalance between the production of reactive oxygen species (ROS) and the body's ability to neutralize them.
This condition can lead to cellular damage and has been implicated in a wide range of diseases, including cardiovascular disorders, neurodegenerative conditions, and cancer.
Optimizing research in this area is crucial for developing effective therapies and preventive strategies.
PubCompare.ai's AI-driven platform can help researchers easily locate relevant protocols from literature, preprints, and patents, then use intelligent comparisons to identify the best methods and products.
This innovative solution can enhance the reproducibility and accuracy of oxidative stress studies, empowering researchers to discover the power of AI-fueled research optimization.
Researchers can utilize tools like CM-H2DCFDA, a fluorescent probe used to detect intracellular ROS, and the Muse Oxidative Stress Kit, which measures oxidative stress markers like glutathione and superoxide.
The TBARS assay kit can be used to quantify lipid peroxidation, a key indicator of oxidative damage.
CellROX Green Reagent is another fluorescent probe that detects oxidative stress in live cells.
Paraquat, a herbicide, is commonly used to induce oxidative stress in experimental models.
The RT2 First Strand Kit can be used for cDNA synthesis, enabling researchers to study gene expression changes in oxidative stress responses.
DCFH-DA is a fluorescent dye that can measure intracellular ROS levels, while the RNeasy Mini Kit can be used for RNA extraction and purification.
By leveraging these tools and techniques, along with PubCompare.ai's AI-powered platform, researchers can enhance the reproducibility and accuracy of their oxidative stress studies, leading to more robust findings and accelerating the development of effective therapies and preventive strategies.