Influence of dietary fat on oxidative stress and inflammation in murine macrophages

Nutrition ◽  
2009 ◽  
Vol 25 (5) ◽  
pp. 548-554 ◽  
Author(s):  
Rocío de la Puerta ◽  
Ana Marquez-Martin ◽  
Angeles Fernandez-Arche ◽  
Valentina Ruiz-Gutierrez
Keyword(s):  
Oxidative Stress ◽  
Dietary Fat ◽  
Murine Macrophages

Oxidative stress induced by P2X7 receptor stimulation in murine macrophages is mediated by c-Src/Pyk2 and ERK1/2

2013 ◽  
Vol 1830 (10) ◽  
pp. 4650-4659 ◽  
Author(s):  
Guadalupe Martel-Gallegos ◽  
Griselda Casas-Pruneda ◽  
Filiberta Ortega-Ortega ◽  
Sergio Sánchez-Armass ◽  
Jesús Alberto Olivares-Reyes ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
P2x7 Receptor ◽  
Receptor Stimulation ◽  
Murine Macrophages

N-Acetyl-tryptophan glucoside (NATG) protects J774A.1 murine macrophages against gamma radiation-induced cell death by modulating oxidative stress

2018 ◽  
Vol 447 (1-2) ◽  
pp. 9-19 ◽  
Author(s):  
Poonam Malhotra ◽  
Ashutosh K. Gupta ◽  
Darshana Singh ◽  
Saurabh Mishra ◽  
Shravan K. Singh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Gamma Radiation ◽  
Murine Macrophages ◽  
Radiation Induced

Abstract 253: Di-n-butyl Phthalate: An Indoor Pollutant Induces Murine Macrophages Oxidative Stress and Inflammation, a Potential Atheropathogenesis Modulator

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Zahra Mazhar ◽  
Dhuha Alsayrafi ◽  
Tong Wu ◽  
Mahdi Garelnabi
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Tnf Alpha ◽  
Gene Expressions ◽  
Compensatory Response ◽  
Murine Macrophages ◽  
Atherosclerosis Progression ◽  
Indoor Pollutant ◽  
Human Cardiovascular System ◽  
Butyl Phthalate

Di-n-butyl phthalate (DBP) is used in air fresheners. It is a colorless oily compound which also used for manufacturing bendable plastics. DBP can cause low acute or chronic toxicity; however, the effect of DBP on humans in the form of air fresheners is not well studied. The effect of DBP on the human cardiovascular system has not been studied. Macrophages are involved in atherosclerosis progression and development; murine macrophages (RAW 264.7) were used for this study. The macrophages were treated with 10uM, 20uM and 50uM DBP for 6 hours, 12 hours and 24 hours. Genes involved in inflammation and antioxidant activity like TNF-a, MCP-1, VCAM-1, NF-kB, PON1, SOCS were analyzed after treatment. macrophages showed statistically significant increases in TNF-alpha expression (p≤ 0.05) after 24 hour treatment with DBP. The expression of NF-kB showed a significant increase in response to DBP treatment (p≤ 0.05) at 24 hours. MCP-1 and VCAM-1 gene expressions were also upregulated after exposure to DBP. Interestingly, catalase gene expression was upregulated in all treatments after 24 hours of exposure however PON-1 gene expression showed differential upregulation responses. Our data clearly suggest that DBP induces inflammation in macrophages. PON1 and catalase upregulated gene expression indicative of a compensatory response to oxidative stress associated with the treatment. Oxidative stress and inflammation mediated macrophages responses strongly linked to atherosclerosis pathogenesis.

scholarly journals Effects of dietary fat modification on oxidative stress and inflammatory markers in the LIPGENE study

2010 ◽  
Vol 104 (9) ◽  
pp. 1357-1362 ◽  
Author(s):  
Helena Petersson ◽  
Ulf Risérus ◽  
Jolene McMonagle ◽  
Hanne L. Gulseth ◽  
Audrey C. Tierney ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dietary Fat ◽  
Dietary Intervention ◽  
Stress Indicator ◽  
Reactive Protein ◽  
The Metabolic Syndrome ◽  
Markers Of Oxidative Stress ◽  
Fat Diets ◽  
The Impact ◽  
And Oxidative Stress

Subjects with the metabolic syndrome (MetS) have enhanced oxidative stress and inflammation. Dietary fat quality has been proposed to be implicated in these conditions. We investigated the impact of four diets distinct in fat quantity and quality on 8-iso-PGF2α (a major F2-isoprostane and oxidative stress indicator), 15-keto-13,14-dihydro-PGF2α (15-keto-dihydro-PGF2α, a major PGF2α metabolite and marker of cyclooxygenase-mediated inflammation) and C-reactive protein (CRP). In a 12-week parallel multicentre dietary intervention study (LIPGENE), 417 volunteers with the MetS were randomly assigned to one of the four diets: two high-fat diets (38 % energy (%E)) rich in SFA or MUFA and two low-fat high-complex carbohydrate diets (28 %E) with (LFHCC n-3) or without (LFHCC) 1·24 g/d of very long chain n-3 fatty acid supplementation. Urinary levels of 8-iso-PGF2α and 15-keto-dihydro-PGF2α were determined by RIA and adjusted for urinary creatinine levels. Serum concentration of CRP was measured by ELISA. Neither concentrations of 8-iso-PGF2α and 15-keto-dihydro-PGF2α nor those of CRP differed between diet groups at baseline (P>0·07) or at the end of the study (P>0·44). Also, no differences in changes of the markers were observed between the diet groups (8-iso-PGF2α, P = 0·83; 15-keto-dihydro-PGF2α, P = 0·45; and CRP, P = 0·97). In conclusion, a 12-week dietary fat modification did not affect the investigated markers of oxidative stress and inflammation among subjects with the MetS in the LIPGENE study.

Oxidative Stress Increases Surface Toll-Like Receptor 4 Expression in Murine Macrophages Via Ceramide Generation

Shock ◽  
2015 ◽  
Vol 44 (2) ◽  
pp. 157-165 ◽  
Author(s):  
Patrick S. Tawadros ◽  
Kinga A. Powers ◽  
Menachem Ailenberg ◽  
Simone E. Birch ◽  
John C. Marshall ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Murine Macrophages ◽  
Ceramide Generation

scholarly journals Catalase-dependent H2O2consumption by cardiac mitochondria and redox-mediated loss in insulin signaling

2016 ◽  
Vol 311 (5) ◽  
pp. H1091-H1096 ◽  
Author(s):  
Paul M. Rindler ◽  
Angela Cacciola ◽  
Michael Kinter ◽  
Luke I. Szweda
Keyword(s):  
Oxidative Stress ◽  
Glutathione Peroxidase ◽  
Binding Affinity ◽  
Insulin Signaling ◽  
Dietary Fat ◽  
High Fat Diet ◽  
Cardiac Mitochondria ◽  
High Fat ◽  
Akt Phosphorylation ◽  
Selective Increase

We have recently demonstrated that catalase content in mouse cardiac mitochondria is selectively elevated in response to high dietary fat, a nutritional state associated with oxidative stress and loss in insulin signaling. Catalase and various isoforms of glutathione peroxidase and peroxiredoxin each catalyze the consumption of H2O2. Catalase, located primarily within peroxisomes and to a lesser extent mitochondria, has a low binding affinity for H2O2relative to glutathione peroxidase and peroxiredoxin. As such, the contribution of catalase to mitochondrial H2O2consumption is not well understood. In the current study, using highly purified cardiac mitochondria challenged with micromolar concentrations of H2O2, we found that catalase contributes significantly to mitochondrial H2O2consumption. In addition, catalase is solely responsible for removal of H2O2in nonrespiring or structurally disrupted mitochondria. Finally, in mice fed a high-fat diet, mitochondrial-derived H2O2is responsible for diminished insulin signaling in the heart as evidenced by reduced insulin-stimulated Akt phosphorylation. While elevated mitochondrial catalase content (∼50%) enhanced the capacity of mitochondria to consume H2O2in response to high dietary fat, the selective increase in catalase did not prevent H2O2-induced loss in cardiac insulin signaling. Taken together, our results indicate that mitochondrial catalase likely functions to preclude the formation of high levels of H2O2without perturbing redox-dependent signaling.

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