ros glo h2 o2 assay  (Promega)

 
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    Name:
    ROS Glo H2O2 Assay
    Description:
    Sensitive bioluminescent assay that measures the level of H2O2 in cell cultures
    Catalog Number:
    g8820
    Price:
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    Category:
    Cell Biology Cell Health Oxidative Stress Assays
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    Structured Review

    Promega ros glo h2 o2 assay
    Effects of hyperoxia on cell viability, proliferation, and reactive oxygen species (H 2 O 2 ) production in male and female HUVECs. Male and Female HUVECs exposed to room air (RA) (room air-5% CO 2 ) and 24, 48, or 72 h of hyperoxia (HO) (95% O 2 -5% CO 2 ) were subjected to trypan blue exclusion (A) or CCK8 assay (B) or <t>ROS-Glo</t> ™ luminescent H 2 O 2 assay to measure the oxidative stress (C) as described in materials and methods. Values are means ± SEM. Significant differences between baseline and subsequent time-points within the same sex are indicated by ** P
    Sensitive bioluminescent assay that measures the level of H2O2 in cell cultures
    https://www.bioz.com/result/ros glo h2 o2 assay/product/Promega
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ros glo h2 o2 assay - by Bioz Stars, 2021-03
    98/100 stars

    Images

    1) Product Images from "Differential Sex-Specific Effects of Oxygen Toxicity in Human Umbilical Vein Endothelial Cells"

    Article Title: Differential Sex-Specific Effects of Oxygen Toxicity in Human Umbilical Vein Endothelial Cells

    Journal: Biochemical and biophysical research communications

    doi: 10.1016/j.bbrc.2017.03.058

    Effects of hyperoxia on cell viability, proliferation, and reactive oxygen species (H 2 O 2 ) production in male and female HUVECs. Male and Female HUVECs exposed to room air (RA) (room air-5% CO 2 ) and 24, 48, or 72 h of hyperoxia (HO) (95% O 2 -5% CO 2 ) were subjected to trypan blue exclusion (A) or CCK8 assay (B) or ROS-Glo ™ luminescent H 2 O 2 assay to measure the oxidative stress (C) as described in materials and methods. Values are means ± SEM. Significant differences between baseline and subsequent time-points within the same sex are indicated by ** P
    Figure Legend Snippet: Effects of hyperoxia on cell viability, proliferation, and reactive oxygen species (H 2 O 2 ) production in male and female HUVECs. Male and Female HUVECs exposed to room air (RA) (room air-5% CO 2 ) and 24, 48, or 72 h of hyperoxia (HO) (95% O 2 -5% CO 2 ) were subjected to trypan blue exclusion (A) or CCK8 assay (B) or ROS-Glo ™ luminescent H 2 O 2 assay to measure the oxidative stress (C) as described in materials and methods. Values are means ± SEM. Significant differences between baseline and subsequent time-points within the same sex are indicated by ** P

    Techniques Used: CCK-8 Assay

    2) Product Images from "c-Jun N-terminal kinase (JNK)-mediated phosphorylation of SARM1 regulates NAD+ cleavage activity to inhibit mitochondrial respiration"

    Article Title: c-Jun N-terminal kinase (JNK)-mediated phosphorylation of SARM1 regulates NAD+ cleavage activity to inhibit mitochondrial respiration

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.RA118.004578

    Inhibition of mitochondrial respiration by SARM1 overexpression. A , schematic representation of human SARM1. MTS, mitochondrial targeting signal; ARM, armadillo/HEAT motifs; SAM, sterile alpha motif; TIR, Toll/interleukin-1 receptor. HEK293T cells were transfected with FLAG-tagged full-length SARM1 or various domain-deletion mutants for 24 h. B , SARM1 overexpression induces reduction of NAD + in HEK293T cells. NAD + level was analyzed by the NAD/NADH-Glo assay. C , SARM1 overexpression induces reduction of ATP in HEK293T cells. ATP level was analyzed by the CellTiter-Glo assay. D , measurements of OCR. At 8 h post transfection, the cells were re-seeded in XF96 plates and further incubated for 16 h. OCR measurements were performed using an XF96 extracellular flux analyzer. E , SARM1 overexpression induces ROS production. ROS level was analyzed by ROS-Glo H 2 O 2 assay. F and G , supplementation of NR prevents SARM1-induced NAD + and ATP reduction. H and I , treatment with the NAMPT inhibitor FK866 enhances SARM1-induced NAD + and ATP reduction. Data represent the mean ± S.D. of three independent experiments. *, p
    Figure Legend Snippet: Inhibition of mitochondrial respiration by SARM1 overexpression. A , schematic representation of human SARM1. MTS, mitochondrial targeting signal; ARM, armadillo/HEAT motifs; SAM, sterile alpha motif; TIR, Toll/interleukin-1 receptor. HEK293T cells were transfected with FLAG-tagged full-length SARM1 or various domain-deletion mutants for 24 h. B , SARM1 overexpression induces reduction of NAD + in HEK293T cells. NAD + level was analyzed by the NAD/NADH-Glo assay. C , SARM1 overexpression induces reduction of ATP in HEK293T cells. ATP level was analyzed by the CellTiter-Glo assay. D , measurements of OCR. At 8 h post transfection, the cells were re-seeded in XF96 plates and further incubated for 16 h. OCR measurements were performed using an XF96 extracellular flux analyzer. E , SARM1 overexpression induces ROS production. ROS level was analyzed by ROS-Glo H 2 O 2 assay. F and G , supplementation of NR prevents SARM1-induced NAD + and ATP reduction. H and I , treatment with the NAMPT inhibitor FK866 enhances SARM1-induced NAD + and ATP reduction. Data represent the mean ± S.D. of three independent experiments. *, p

    Techniques Used: Inhibition, Over Expression, Transfection, Glo Assay, Incubation

    3) Product Images from "c-Jun N-terminal kinase (JNK)-mediated phosphorylation of SARM1 regulates NAD+ cleavage activity to inhibit mitochondrial respiration"

    Article Title: c-Jun N-terminal kinase (JNK)-mediated phosphorylation of SARM1 regulates NAD+ cleavage activity to inhibit mitochondrial respiration

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.RA118.004578

    Inhibition of mitochondrial respiration by SARM1 overexpression. A , schematic representation of human SARM1. MTS, mitochondrial targeting signal; ARM, armadillo/HEAT motifs; SAM, sterile alpha motif; TIR, Toll/interleukin-1 receptor. HEK293T cells were transfected with FLAG-tagged full-length SARM1 or various domain-deletion mutants for 24 h. B , SARM1 overexpression induces reduction of NAD + in HEK293T cells. NAD + level was analyzed by the NAD/NADH-Glo assay. C , SARM1 overexpression induces reduction of ATP in HEK293T cells. ATP level was analyzed by the CellTiter-Glo assay. D , measurements of OCR. At 8 h post transfection, the cells were re-seeded in XF96 plates and further incubated for 16 h. OCR measurements were performed using an XF96 extracellular flux analyzer. E , SARM1 overexpression induces ROS production. ROS level was analyzed by ROS-Glo H 2 O 2 assay. F and G , supplementation of NR prevents SARM1-induced NAD + and ATP reduction. H and I , treatment with the NAMPT inhibitor FK866 enhances SARM1-induced NAD + and ATP reduction. Data represent the mean ± S.D. of three independent experiments. *, p
    Figure Legend Snippet: Inhibition of mitochondrial respiration by SARM1 overexpression. A , schematic representation of human SARM1. MTS, mitochondrial targeting signal; ARM, armadillo/HEAT motifs; SAM, sterile alpha motif; TIR, Toll/interleukin-1 receptor. HEK293T cells were transfected with FLAG-tagged full-length SARM1 or various domain-deletion mutants for 24 h. B , SARM1 overexpression induces reduction of NAD + in HEK293T cells. NAD + level was analyzed by the NAD/NADH-Glo assay. C , SARM1 overexpression induces reduction of ATP in HEK293T cells. ATP level was analyzed by the CellTiter-Glo assay. D , measurements of OCR. At 8 h post transfection, the cells were re-seeded in XF96 plates and further incubated for 16 h. OCR measurements were performed using an XF96 extracellular flux analyzer. E , SARM1 overexpression induces ROS production. ROS level was analyzed by ROS-Glo H 2 O 2 assay. F and G , supplementation of NR prevents SARM1-induced NAD + and ATP reduction. H and I , treatment with the NAMPT inhibitor FK866 enhances SARM1-induced NAD + and ATP reduction. Data represent the mean ± S.D. of three independent experiments. *, p

    Techniques Used: Inhibition, Over Expression, Transfection, Glo Assay, Incubation

    4) Product Images from "Comparative Gene Expression Analysis in WM164 Melanoma Cells Revealed That β-β-Dimethylacrylshikonin Leads to ROS Generation, Loss of Mitochondrial Membrane Potential, and Autophagy Induction"

    Article Title: Comparative Gene Expression Analysis in WM164 Melanoma Cells Revealed That β-β-Dimethylacrylshikonin Leads to ROS Generation, Loss of Mitochondrial Membrane Potential, and Autophagy Induction

    Journal: Molecules

    doi: 10.3390/molecules23112823

    Results of the ROS-Glo™ assay. A : SBcl2, B : WM9, and C : WM164 cells treated with the respective IC 50 of DMAS in the absence or presence of 1 µg/mL catalase (cat) or 1 mM pyruvate (pyr) for 4 h. D : WM164 cells treated with menadione (positive control) in the absence or presence of 1 µg/mL catalase (cat) or 1 mM pyruvate (pyr). Results are displayed as mean ± sem ( n = 6).
    Figure Legend Snippet: Results of the ROS-Glo™ assay. A : SBcl2, B : WM9, and C : WM164 cells treated with the respective IC 50 of DMAS in the absence or presence of 1 µg/mL catalase (cat) or 1 mM pyruvate (pyr) for 4 h. D : WM164 cells treated with menadione (positive control) in the absence or presence of 1 µg/mL catalase (cat) or 1 mM pyruvate (pyr). Results are displayed as mean ± sem ( n = 6).

    Techniques Used: Glo Assay, Positive Control

    5) Product Images from "Development of novel amino-quinoline-5,8-dione derivatives as NAD(P)H:quinone oxidoreductase 1 (NQO1) inhibitors with potent antiproliferative activities"

    Article Title: Development of novel amino-quinoline-5,8-dione derivatives as NAD(P)H:quinone oxidoreductase 1 (NQO1) inhibitors with potent antiproliferative activities

    Journal: European journal of medicinal chemistry

    doi: 10.1016/j.ejmech.2018.05.025

    Reactive oxygen species (ROS) generation of (a) HeLa cells (b) KB-vin cells after compound treatment. The HeLa and KB-vin cells were treated with serial concentrations of PL, 6h, 6d, 7a, and 7d for 24 h. The generated ROS were detected by the ROS-Glo™ H 2 O 2 assay kit (catalog number: G8821), and increased significantly after treatment with 6h, 6d, 7a, and 7d for 24 h.
    Figure Legend Snippet: Reactive oxygen species (ROS) generation of (a) HeLa cells (b) KB-vin cells after compound treatment. The HeLa and KB-vin cells were treated with serial concentrations of PL, 6h, 6d, 7a, and 7d for 24 h. The generated ROS were detected by the ROS-Glo™ H 2 O 2 assay kit (catalog number: G8821), and increased significantly after treatment with 6h, 6d, 7a, and 7d for 24 h.

    Techniques Used: Generated

    6) Product Images from "Nanoliposome C6-Ceramide Increases the Anti-tumor Immune Response and Slows Growth of Liver Tumors in Mice"

    Article Title: Nanoliposome C6-Ceramide Increases the Anti-tumor Immune Response and Slows Growth of Liver Tumors in Mice

    Journal: Gastroenterology

    doi: 10.1053/j.gastro.2017.10.050

    LipC6 administration suppresses O 2− generation in TAMs and BMMs. Size-matched TBMs were randomly assigned to 1 of 3 groups: vehicle, LipC6, or no injection. Two weeks after injection, splenic leukocytes and TILs were prepared from the spleen and the perfused tumors. The cells were incubated for 45 minutes at 37°C, then washed 3 times with media, with the remaining adherent cells being > 90% CD11b positive (macrophages). Intracellular ROS were measured with Glo H 2 O 2 assay. Briefly, H 2 O 2 substrate was added to each well followed by addition of ROS-Glo detection solution. After incubation for 20 minutes at room temperature, relative luminescence was measured to assess ROS level in TAMs ( A ) and splenic macrophages ( B ). Similarly, BMMs were prepared in vitro by stimulating bone marrow cells from wild-type C57BL/6 mice with GMCSF (G-BMMs) and MCSF (M-BMMs) for 6 days. After incubation with LipC6 or vehicle overnight, the relative ROS level in G-BMMs ( C ) and M-BMMs ( D ) were measured. n = 3; error bars represent ± SD. * P
    Figure Legend Snippet: LipC6 administration suppresses O 2− generation in TAMs and BMMs. Size-matched TBMs were randomly assigned to 1 of 3 groups: vehicle, LipC6, or no injection. Two weeks after injection, splenic leukocytes and TILs were prepared from the spleen and the perfused tumors. The cells were incubated for 45 minutes at 37°C, then washed 3 times with media, with the remaining adherent cells being > 90% CD11b positive (macrophages). Intracellular ROS were measured with Glo H 2 O 2 assay. Briefly, H 2 O 2 substrate was added to each well followed by addition of ROS-Glo detection solution. After incubation for 20 minutes at room temperature, relative luminescence was measured to assess ROS level in TAMs ( A ) and splenic macrophages ( B ). Similarly, BMMs were prepared in vitro by stimulating bone marrow cells from wild-type C57BL/6 mice with GMCSF (G-BMMs) and MCSF (M-BMMs) for 6 days. After incubation with LipC6 or vehicle overnight, the relative ROS level in G-BMMs ( C ) and M-BMMs ( D ) were measured. n = 3; error bars represent ± SD. * P

    Techniques Used: Injection, Incubation, In Vitro, Mouse Assay

    7) Product Images from "NRF2 Regulates PINK1 Expression under Oxidative Stress Conditions"

    Article Title: NRF2 Regulates PINK1 Expression under Oxidative Stress Conditions

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0142438

    Involvement of ROS in induction of PINK1 expression by NRF2. (A) Overexpression of KEAP1 suppresses PINK1 expression induced by tBHQ. SH-SY5Y cells were transfected with N-terminal HA-tagged KEAP1 along with PINK1 pro-luc and GFP for 24 h followed by treatment with 40 μM tBHQ for 48 h. PINK1 promoter activity was measured by a luciferase assay. (B) An ROS scavenger, NAC, inhibits production of H 2 O 2 induced by chemicals. SH-SY5Y cells were treated with 2 mM NAC along with designated compounds for 6 h. H 2 O 2 was detected using an ROS-Glo H 2 O 2 assay. (C-E) NAC inhibits induction of PINK1 expression induced by 40 μM tBHQ (C), 20 μM 6-OHDA (D) or 20 μM CdCl 2 (E). These experiments were performed under conditions similar to those described in (A). *, p
    Figure Legend Snippet: Involvement of ROS in induction of PINK1 expression by NRF2. (A) Overexpression of KEAP1 suppresses PINK1 expression induced by tBHQ. SH-SY5Y cells were transfected with N-terminal HA-tagged KEAP1 along with PINK1 pro-luc and GFP for 24 h followed by treatment with 40 μM tBHQ for 48 h. PINK1 promoter activity was measured by a luciferase assay. (B) An ROS scavenger, NAC, inhibits production of H 2 O 2 induced by chemicals. SH-SY5Y cells were treated with 2 mM NAC along with designated compounds for 6 h. H 2 O 2 was detected using an ROS-Glo H 2 O 2 assay. (C-E) NAC inhibits induction of PINK1 expression induced by 40 μM tBHQ (C), 20 μM 6-OHDA (D) or 20 μM CdCl 2 (E). These experiments were performed under conditions similar to those described in (A). *, p

    Techniques Used: Expressing, Over Expression, Transfection, Activity Assay, Luciferase

    8) Product Images from "Induction of DNA Damages upon Marek's Disease Virus Infection: Implication in Viral Replication and Pathogenesis"

    Article Title: Induction of DNA Damages upon Marek's Disease Virus Infection: Implication in Viral Replication and Pathogenesis

    Journal: Journal of Virology

    doi: 10.1128/JVI.01658-17

    MDV replication induces production of ROS and NO. CESCs were mock infected or infected with recEGFPVP22. (A) ROS accumulation in the supernatants of mock- and recEGFPVP22-infected cells. At 24, 48, 72, and 96 hpi, the supernatants of mock- and recEGFPVP22-infected cells were collected, and the level of H 2 O 2 accumulation was quantified using an ROS-Glo kit (Promega). Results were normalized to the RLU values obtained from mock-infected cells and are expressed as means ± SDs. (B) NO production in the supernatants of mock- and recEGFPVP22-infected cells. At the indicated time points, the supernatants of mock- and recEGFPVP22-infected cells were collected, and nitrite accumulation was quantified using the Griess reaction. Results are presented as the mean fold change in the level of NO 2 − in the supernatants of infected cells relative to that in the supernatants of mock-infected cells ± SDs. ***, P
    Figure Legend Snippet: MDV replication induces production of ROS and NO. CESCs were mock infected or infected with recEGFPVP22. (A) ROS accumulation in the supernatants of mock- and recEGFPVP22-infected cells. At 24, 48, 72, and 96 hpi, the supernatants of mock- and recEGFPVP22-infected cells were collected, and the level of H 2 O 2 accumulation was quantified using an ROS-Glo kit (Promega). Results were normalized to the RLU values obtained from mock-infected cells and are expressed as means ± SDs. (B) NO production in the supernatants of mock- and recEGFPVP22-infected cells. At the indicated time points, the supernatants of mock- and recEGFPVP22-infected cells were collected, and nitrite accumulation was quantified using the Griess reaction. Results are presented as the mean fold change in the level of NO 2 − in the supernatants of infected cells relative to that in the supernatants of mock-infected cells ± SDs. ***, P

    Techniques Used: Infection

    9) Product Images from "MIF/CD74 axis is a target for novel therapies in colon carcinomatosis"

    Article Title: MIF/CD74 axis is a target for novel therapies in colon carcinomatosis

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    doi: 10.1186/s13046-016-0475-z

    Mitochondria impairment after 4-IPP and metformin treatments in C2 organoids. a Reactive oxygen species detection with ROS-H2O2-Glo assay kit. C2 cells were treated with metformin 5 mM, 4-IPP 100 μM or left untreated for 120 and 24 h respectively. Extracellular H2O2 formation was detected and quantified using the ROS-H2O2-Glo assay. Luminescence intensity was quantified using a microplate reader with a 500 ms integration time, reported as relative light units and normalised to 0 cells/well treatment conditions. Standard deviation was calculated for a set of triplicate values. b Confocal microscopy images of mitochondria using Mitotracker® Deep Red FM in C2 cells untreated ( A2 ; D1 ; E1 ), treated with 50 μM 4-IPP for 24 h ( B2 ), 100 μM 4-IPP for 24 h ( C2 ), or 5 mM metformin for 120 h ( D2 ; E2 ). Arrows indicate aggregated mitochondria. 4-IPP treatment leads to mitochondria impairment in C2 cells. Metformin treatment reduces signal intensity of Mitotracker (asterisk) suggesting a depolarization of mitochondrial membrane potential. The figure shows data from a representative experiment. DIC: differential interference contrast. Magnifications: 10X. Scale bars = 50 μm. All the experiments were replicated at least three times. C Flow cytometry analysis of the mitochondrial membrane potential using JC-1 assay on C2 organoids treated with metformin for 120 h or left untreated. Staining JC-1 revealed that metformin treatment caused a significant increase in the amount of FITC aggregates, a pattern that is characteristic for disruption of mitochondrial membrane potential. d The ultrastructure of the C2 cells after 4-IPP ( D1-3 ) or metformin treatment ( D4-6 ) and left untreated ( D7 ). The white arrows show autophagic structures and red stars indicate apoptotic bodies present in 4-IPP treated cells. White triangles show irregular mitochondria, blue stars lipid droplets and the yellow star a multilamellar structure present in metformin treated cells. Additionally, no signs of autophagy, apoptosis or irregular mitochondria were observed in untreated cells ( D7 ). e Functional consequences of 4-IPP or metformin treatments on C2 organoids
    Figure Legend Snippet: Mitochondria impairment after 4-IPP and metformin treatments in C2 organoids. a Reactive oxygen species detection with ROS-H2O2-Glo assay kit. C2 cells were treated with metformin 5 mM, 4-IPP 100 μM or left untreated for 120 and 24 h respectively. Extracellular H2O2 formation was detected and quantified using the ROS-H2O2-Glo assay. Luminescence intensity was quantified using a microplate reader with a 500 ms integration time, reported as relative light units and normalised to 0 cells/well treatment conditions. Standard deviation was calculated for a set of triplicate values. b Confocal microscopy images of mitochondria using Mitotracker® Deep Red FM in C2 cells untreated ( A2 ; D1 ; E1 ), treated with 50 μM 4-IPP for 24 h ( B2 ), 100 μM 4-IPP for 24 h ( C2 ), or 5 mM metformin for 120 h ( D2 ; E2 ). Arrows indicate aggregated mitochondria. 4-IPP treatment leads to mitochondria impairment in C2 cells. Metformin treatment reduces signal intensity of Mitotracker (asterisk) suggesting a depolarization of mitochondrial membrane potential. The figure shows data from a representative experiment. DIC: differential interference contrast. Magnifications: 10X. Scale bars = 50 μm. All the experiments were replicated at least three times. C Flow cytometry analysis of the mitochondrial membrane potential using JC-1 assay on C2 organoids treated with metformin for 120 h or left untreated. Staining JC-1 revealed that metformin treatment caused a significant increase in the amount of FITC aggregates, a pattern that is characteristic for disruption of mitochondrial membrane potential. d The ultrastructure of the C2 cells after 4-IPP ( D1-3 ) or metformin treatment ( D4-6 ) and left untreated ( D7 ). The white arrows show autophagic structures and red stars indicate apoptotic bodies present in 4-IPP treated cells. White triangles show irregular mitochondria, blue stars lipid droplets and the yellow star a multilamellar structure present in metformin treated cells. Additionally, no signs of autophagy, apoptosis or irregular mitochondria were observed in untreated cells ( D7 ). e Functional consequences of 4-IPP or metformin treatments on C2 organoids

    Techniques Used: Glo Assay, Mass Spectrometry, Standard Deviation, Confocal Microscopy, Flow Cytometry, Cytometry, Staining, Functional Assay

    10) Product Images from "Mechanisms of growth inhibition of primary prostate epithelial cells following gamma irradiation or photodynamic therapy include senescence, necrosis, and autophagy, but not apoptosis"

    Article Title: Mechanisms of growth inhibition of primary prostate epithelial cells following gamma irradiation or photodynamic therapy include senescence, necrosis, and autophagy, but not apoptosis

    Journal: Cancer Medicine

    doi: 10.1002/cam4.553

    Increasing doses of photodynamic therapy ( PDT ) drug or gamma irradiation results in a reduction and ablation of colony‐forming ability in primary prostate epithelial cells and an increase in production of Reactive Oxygen Species ( ROS ). Primary prostate epithelial cells from four patients were treated with varying doses of PDT drug (A) or gamma irradiation (B), and the colony‐forming ability was assessed after 7 days of growth. Colony‐forming ability is presented as % surviving fraction. Primary prostate epithelial cells were treated with increasing doses of (C) PDT drug or (D) gamma irradiation and the production of ROS was measured using the ROS ‐Glo assay (Promega).
    Figure Legend Snippet: Increasing doses of photodynamic therapy ( PDT ) drug or gamma irradiation results in a reduction and ablation of colony‐forming ability in primary prostate epithelial cells and an increase in production of Reactive Oxygen Species ( ROS ). Primary prostate epithelial cells from four patients were treated with varying doses of PDT drug (A) or gamma irradiation (B), and the colony‐forming ability was assessed after 7 days of growth. Colony‐forming ability is presented as % surviving fraction. Primary prostate epithelial cells were treated with increasing doses of (C) PDT drug or (D) gamma irradiation and the production of ROS was measured using the ROS ‐Glo assay (Promega).

    Techniques Used: Irradiation, Glo Assay

    Related Articles

    H2O2 Assay:

    Article Title: Induction of DNA Damages upon Marek's Disease Virus Infection: Implication in Viral Replication and Pathogenesis
    Article Snippet: Results are presented as the mean OTM ± standard deviation (SD) calculated for each condition or as a distribution of the comets with respect to their respective OTM value (i.e., the percentage of cells presenting a defined OTM). .. Reactive oxygen species (ROS) production was assayed from the supernatants (80 μl) of mock- and recEGFPVP22-infected CESCs at 24, 48, 72, and 96 hpi using an ROS-Glo H2 O2 assay following the manufacturer's instructions (Promega). .. Luminescence quantification was performed using a Glomax multidetection system luminometer (Promega).

    Article Title: Development of novel amino-quinoline-5,8-dione derivatives as NAD(P)H:quinone oxidoreductase 1 (NQO1) inhibitors with potent antiproliferative activities
    Article Snippet: To calculate the kinetic parameters of inhibition mechanism of NQO1, steady-state rates were obtained at various concentrations of test compounds and substrate. .. The ROS-Glo H2 O2 Assay (Promega® , Southampton, UK) was used to measure changes of ROS by directly detecting H2 O2 in cells. .. The cells were plated in 96-well white tissue culture plates and then treated with test compounds (0.01 µM−5 µM) for 24 h. The H2 O2 substrate solution was added to each well and incubated for 6h at 37 °C in a CO2 incubator.

    Article Title: Comparative Gene Expression Analysis in WM164 Melanoma Cells Revealed That β-β-Dimethylacrylshikonin Leads to ROS Generation, Loss of Mitochondrial Membrane Potential, and Autophagy Induction
    Article Snippet: .. ROS-Glo™ H2 O2 Assay The ROS-Glo™ H2 O2 Assay from Promega (Mannheim, Germany) was performed in accordance with the manufacturer’s instructions. .. Afterwards, medium was replaced by 75 µL RPMI medium, RPMI medium with 1 mM sodium pyruvate, or RPMI medium with 100 µg/mL (350 U/mL) catalase (Sigma-Aldrich) each containing 2% FBS and 1% Pen/Strep.

    Article Title: Nanoliposome C6-Ceramide Increases the Anti-tumor Immune Response and Slows Growth of Liver Tumors in Mice
    Article Snippet: The level of IFN-γ in cell culture supernatant was measured with mouse Quantikine ELISA Kits (Cat # DY485, R & D System) according to the manufacturer’s instructions. .. ROS level was detected and quantified using the ROS-Glo H2 O2 Assay (Promega, Madison, WI) according to the manufacturer’s protocol. .. Briefly, cells were grown in 96-well plate until 80% confluence followed by the incubation with LipC6 or vehicle for 6 hours, the H2 O2 substrate was added to each well and incubated in 37°C, 5% CO2 incubator for desired time, then ROS-Glo detection solution was added and incubated for 20 minutes at room temperature.

    Article Title: Mechanisms of growth inhibition of primary prostate epithelial cells following gamma irradiation or photodynamic therapy include senescence, necrosis, and autophagy, but not apoptosis
    Article Snippet: .. ROS‐Glo H2 O2 assay In order to measure production of H2 O2 , one of the most stable reactive oxygen species and the end product of other ROS enzyme reactions , the ROS‐Glo H2 O2 Assay (Promega G8820, Southampton, UK) was carried out. ..

    Article Title: Low-temperature plasma treatment induces DNA damage leading to necrotic cell death in primary prostate epithelial cells
    Article Snippet: Autocomet software (Tritek Corp., Sumerduck, VA, USA) was used to analyse cell images, with the median percentage of DNA-in-tail values used to record DNA damage in a minimum of 100 cells per treatment. .. Detection of ROS Extracellular H2 O2 formed in the culture media as a result of LTP treatment was detected and quantified using the ROS-Glo H2 O2 assay (Cat. no. G8820, Promega, Southhampton, UK). ..


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    Promega ros glo h2 o2 assay
    Reactive oxygen species <t>(ROS)</t> generation of (a) HeLa cells (b) KB-vin cells after compound treatment. The HeLa and KB-vin cells were treated with serial concentrations of PL, 6h, 6d, 7a, and 7d for 24 h. The generated ROS were detected by the <t>ROS-Glo™</t> H 2 O 2 assay kit (catalog number: G8821), and increased significantly after treatment with 6h, 6d, 7a, and 7d for 24 h.
    Ros Glo H2 O2 Assay, supplied by Promega, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/ros glo h2 o2 assay/product/Promega
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    ros glo h2 o2 assay - by Bioz Stars, 2021-03
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    Reactive oxygen species (ROS) generation of (a) HeLa cells (b) KB-vin cells after compound treatment. The HeLa and KB-vin cells were treated with serial concentrations of PL, 6h, 6d, 7a, and 7d for 24 h. The generated ROS were detected by the ROS-Glo™ H 2 O 2 assay kit (catalog number: G8821), and increased significantly after treatment with 6h, 6d, 7a, and 7d for 24 h.

    Journal: European journal of medicinal chemistry

    Article Title: Development of novel amino-quinoline-5,8-dione derivatives as NAD(P)H:quinone oxidoreductase 1 (NQO1) inhibitors with potent antiproliferative activities

    doi: 10.1016/j.ejmech.2018.05.025

    Figure Lengend Snippet: Reactive oxygen species (ROS) generation of (a) HeLa cells (b) KB-vin cells after compound treatment. The HeLa and KB-vin cells were treated with serial concentrations of PL, 6h, 6d, 7a, and 7d for 24 h. The generated ROS were detected by the ROS-Glo™ H 2 O 2 assay kit (catalog number: G8821), and increased significantly after treatment with 6h, 6d, 7a, and 7d for 24 h.

    Article Snippet: The ROS-Glo H2 O2 Assay (Promega® , Southampton, UK) was used to measure changes of ROS by directly detecting H2 O2 in cells.

    Techniques: Generated

    LipC6 administration suppresses O 2− generation in TAMs and BMMs. Size-matched TBMs were randomly assigned to 1 of 3 groups: vehicle, LipC6, or no injection. Two weeks after injection, splenic leukocytes and TILs were prepared from the spleen and the perfused tumors. The cells were incubated for 45 minutes at 37°C, then washed 3 times with media, with the remaining adherent cells being > 90% CD11b positive (macrophages). Intracellular ROS were measured with Glo H 2 O 2 assay. Briefly, H 2 O 2 substrate was added to each well followed by addition of ROS-Glo detection solution. After incubation for 20 minutes at room temperature, relative luminescence was measured to assess ROS level in TAMs ( A ) and splenic macrophages ( B ). Similarly, BMMs were prepared in vitro by stimulating bone marrow cells from wild-type C57BL/6 mice with GMCSF (G-BMMs) and MCSF (M-BMMs) for 6 days. After incubation with LipC6 or vehicle overnight, the relative ROS level in G-BMMs ( C ) and M-BMMs ( D ) were measured. n = 3; error bars represent ± SD. * P

    Journal: Gastroenterology

    Article Title: Nanoliposome C6-Ceramide Increases the Anti-tumor Immune Response and Slows Growth of Liver Tumors in Mice

    doi: 10.1053/j.gastro.2017.10.050

    Figure Lengend Snippet: LipC6 administration suppresses O 2− generation in TAMs and BMMs. Size-matched TBMs were randomly assigned to 1 of 3 groups: vehicle, LipC6, or no injection. Two weeks after injection, splenic leukocytes and TILs were prepared from the spleen and the perfused tumors. The cells were incubated for 45 minutes at 37°C, then washed 3 times with media, with the remaining adherent cells being > 90% CD11b positive (macrophages). Intracellular ROS were measured with Glo H 2 O 2 assay. Briefly, H 2 O 2 substrate was added to each well followed by addition of ROS-Glo detection solution. After incubation for 20 minutes at room temperature, relative luminescence was measured to assess ROS level in TAMs ( A ) and splenic macrophages ( B ). Similarly, BMMs were prepared in vitro by stimulating bone marrow cells from wild-type C57BL/6 mice with GMCSF (G-BMMs) and MCSF (M-BMMs) for 6 days. After incubation with LipC6 or vehicle overnight, the relative ROS level in G-BMMs ( C ) and M-BMMs ( D ) were measured. n = 3; error bars represent ± SD. * P

    Article Snippet: ROS level was detected and quantified using the ROS-Glo H2 O2 Assay (Promega, Madison, WI) according to the manufacturer’s protocol.

    Techniques: Injection, Incubation, In Vitro, Mouse Assay

    Septic exosome-induced elevation of intracellular ROS in MCECs contributes to the increase of podosome clusters and EC hyperpermeability Septic exosomes were able to increase the intracellular ROS levels in MCECs. ( A ) The ROS levels in septic and non-septic exosomes were measured with ROS-Glo H 2 O 2 Assay Kit. The relative light units (RLU) of luminescence was recorded by microplate reader. ( B ) MCECs were incubated with PMA (80 ng/ml) or equivalent volume of PBS for 0.5 h before conducting ROS assay. ( C and D ) To investigate the role of exosomal ROS, MnT (a scavenger of ROS) was added into septic exosomes to a final concentration of 40 μM at 1 h before applying into MCECs. ECs were then incubated with non-septic exosomes or septic exosomes (with/without MnT) for 1 h. After that, ECs were washed with PBS, and ROS assays were performed. Values are presented as means ± SD (n=6, * P

    Journal: Shock (Augusta, Ga.)

    Article Title: Circulating Exosomes Isolated from Septic Mice Induce Cardiovascular Hyperpermeability through Promoting Podosome Cluster Formation

    doi: 10.1097/SHK.0000000000000928

    Figure Lengend Snippet: Septic exosome-induced elevation of intracellular ROS in MCECs contributes to the increase of podosome clusters and EC hyperpermeability Septic exosomes were able to increase the intracellular ROS levels in MCECs. ( A ) The ROS levels in septic and non-septic exosomes were measured with ROS-Glo H 2 O 2 Assay Kit. The relative light units (RLU) of luminescence was recorded by microplate reader. ( B ) MCECs were incubated with PMA (80 ng/ml) or equivalent volume of PBS for 0.5 h before conducting ROS assay. ( C and D ) To investigate the role of exosomal ROS, MnT (a scavenger of ROS) was added into septic exosomes to a final concentration of 40 μM at 1 h before applying into MCECs. ECs were then incubated with non-septic exosomes or septic exosomes (with/without MnT) for 1 h. After that, ECs were washed with PBS, and ROS assays were performed. Values are presented as means ± SD (n=6, * P

    Article Snippet: Therefore, in the present study, we measured the levels of ROS within exosomes by using ROS-Glo H2 O2 Assay kit (G8820, Promega).

    Techniques: Incubation, ROS Assay, Concentration Assay

    Inhibition of mitochondrial respiration by SARM1 overexpression. A , schematic representation of human SARM1. MTS, mitochondrial targeting signal; ARM, armadillo/HEAT motifs; SAM, sterile alpha motif; TIR, Toll/interleukin-1 receptor. HEK293T cells were transfected with FLAG-tagged full-length SARM1 or various domain-deletion mutants for 24 h. B , SARM1 overexpression induces reduction of NAD + in HEK293T cells. NAD + level was analyzed by the NAD/NADH-Glo assay. C , SARM1 overexpression induces reduction of ATP in HEK293T cells. ATP level was analyzed by the CellTiter-Glo assay. D , measurements of OCR. At 8 h post transfection, the cells were re-seeded in XF96 plates and further incubated for 16 h. OCR measurements were performed using an XF96 extracellular flux analyzer. E , SARM1 overexpression induces ROS production. ROS level was analyzed by ROS-Glo H 2 O 2 assay. F and G , supplementation of NR prevents SARM1-induced NAD + and ATP reduction. H and I , treatment with the NAMPT inhibitor FK866 enhances SARM1-induced NAD + and ATP reduction. Data represent the mean ± S.D. of three independent experiments. *, p

    Journal: The Journal of Biological Chemistry

    Article Title: c-Jun N-terminal kinase (JNK)-mediated phosphorylation of SARM1 regulates NAD+ cleavage activity to inhibit mitochondrial respiration

    doi: 10.1074/jbc.RA118.004578

    Figure Lengend Snippet: Inhibition of mitochondrial respiration by SARM1 overexpression. A , schematic representation of human SARM1. MTS, mitochondrial targeting signal; ARM, armadillo/HEAT motifs; SAM, sterile alpha motif; TIR, Toll/interleukin-1 receptor. HEK293T cells were transfected with FLAG-tagged full-length SARM1 or various domain-deletion mutants for 24 h. B , SARM1 overexpression induces reduction of NAD + in HEK293T cells. NAD + level was analyzed by the NAD/NADH-Glo assay. C , SARM1 overexpression induces reduction of ATP in HEK293T cells. ATP level was analyzed by the CellTiter-Glo assay. D , measurements of OCR. At 8 h post transfection, the cells were re-seeded in XF96 plates and further incubated for 16 h. OCR measurements were performed using an XF96 extracellular flux analyzer. E , SARM1 overexpression induces ROS production. ROS level was analyzed by ROS-Glo H 2 O 2 assay. F and G , supplementation of NR prevents SARM1-induced NAD + and ATP reduction. H and I , treatment with the NAMPT inhibitor FK866 enhances SARM1-induced NAD + and ATP reduction. Data represent the mean ± S.D. of three independent experiments. *, p

    Article Snippet: ROS-Glo H2 O2 assay (Promega Biosciences) was used for an ROS assay.

    Techniques: Inhibition, Over Expression, Transfection, Glo Assay, Incubation