scholarly journals Involvement of Cytochrome P450 1A in the toxicity of aryl hydrocarbon receptor agonists : alteration arachidonic acid metabolism and production of reactive oxygen species

1998 ◽  
Author(s):  
Jennifer J. Schlezinger
Keyword(s):  
Reactive Oxygen Species ◽  
Arachidonic Acid ◽  
Cytochrome P450 ◽  
Aryl Hydrocarbon Receptor ◽  
Acid Metabolism ◽  
Reactive Oxygen ◽  
Arachidonic Acid Metabolism ◽  
Oxygen Species ◽  
Aryl Hydrocarbon ◽  
Cytochrome P450 1A

Role of mitochondrial complexes I and II, reactive oxygen species and arachidonic acid metabolism in deoxycholate-induced apoptosis

2002 ◽  
Vol 177 (2) ◽  
pp. 129-144 ◽  
Author(s):  
Delon Washo-Stultz ◽  
Cara L Crowley-Weber ◽  
Katerina Dvorakova ◽  
Carol Bernstein ◽  
Harris Bernstein ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Reactive Oxygen ◽  
Arachidonic Acid Metabolism ◽  
Oxygen Species ◽  
Mitochondrial Complexes ◽  
Induced Apoptosis

Effects of reactive oxygen species on arachidonic acid metabolism in rabbit platelets

1993 ◽  
Vol 15 (1) ◽  
pp. 101-104 ◽  
Author(s):  
Toshiki Sumiya ◽  
Yohko Fujimoto ◽  
Hiroko Nishida ◽  
Yuriyo Morikawa ◽  
Satotu Sakuma ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Reactive Oxygen ◽  
Arachidonic Acid Metabolism ◽  
Oxygen Species ◽  
Rabbit Platelets

scholarly journals Kosmetik Antipolusi : Kosmetik Zaman Now

2017 ◽  
Vol 2 (5) ◽  
pp. 9
Author(s):  
Eka Riza Maula
Keyword(s):  
Reactive Oxygen Species ◽  
Aryl Hydrocarbon Receptor ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Aryl Hydrocarbon

Polusi di lingkungan mempunyai dampak negatif pada kesehatan manusia. Selain itu, juga menyebabkan dampak negatif terhadap kulit diantaranya, penuaan kulit, pigmentasi kulit, dan jerawat. Paparan polusi juga menjadi isu serius meliputi dermatitis atopik, psoriasis, dan bahkan kanker kulit. Adanya paparan polutan akibat kontaminasi lingkungan akan meningkatkan produksi reactive oxygen species (ROS), aktivasi Aryl hydrocarbon receptor (AhR), dan menginduksi respon inflamasi. Beberapa zat aktif dapat digunakan sebagai bahan antipolusi dan bekerja melalui beberapa cara diantaranya, Membersihkan kulit dan pembentukan lapisan film, Memperkuat lapisan pelindung kulit dan meningkatkan kelembaban, Meningkatkan kandungan Antioksidan, Mencegah degradasi kollagen/Elastin, Kontrol pigmentasi, dan Mengurangi Inflamasi.Kata kunci : Kosmetik, polusi, antioksidan, pigmentasi

scholarly journals Arachidonic acid stimulates TNFα production in Kupffer cells via a reactive oxygen species-pERK1/2-Egr1-dependent mechanism

2012 ◽  
Vol 303 (2) ◽  
pp. G228-G239 ◽  
Author(s):  
Francisco Javier Cubero ◽  
Natalia Nieto
Keyword(s):  
Reactive Oxygen Species ◽  
Fatty Acids ◽  
Arachidonic Acid ◽  
Liver Disease ◽  
Nadph Oxidase ◽  
Alcoholic Liver Disease ◽  
Kupffer Cells ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Oxygen Species

Kupffer cells are a key source of mediators of alcohol-induced liver damage such as reactive oxygen species, chemokines, growth factors, and eicosanoids. Since diets rich in polyunsaturated fatty acids are a requirement for the development of alcoholic liver disease, we hypothesized that polyunsaturated fatty acids could synergize with ethanol to promote Kupffer cell activation and TNFα production, hence, contributing to liver injury. Primary Kupffer cells from control and from ethanol-fed rats incubated with arachidonic acid showed similar proliferation rates than nontreated cells; however, arachidonic acid induced phenotypic changes, lipid peroxidation, hydroperoxides, and superoxide radical generation. Similar effects occurred in human Kupffer cells. These events were greater in Kupffer cells from ethanol-fed rats, and antioxidants and inhibitors of arachidonic acid metabolism prevented them. Arachidonic acid treatment increased NADPH oxidase activity. Inhibitors of NADPH oxidase and of arachidonic acid metabolism partially prevented the increase in oxidant stress. Upon arachidonic acid stimulation, there was a rapid and sustained increase in TNFα, which was greater in Kupffer cells from ethanol-fed rats than in Kupffer cells from control rats. Arachidonic acid induced ERK1/2 phosphorylation and nuclear translocation of early growth response-1 (Egr1), and ethanol synergized with arachidonic acid to promote this effect. PD98059, a mitogen extracellular kinase 1/2 inhibitor, and curcumin, an Egr1 inhibitor, blocked the arachidonic acid-mediated upregulation of TNFα in Kupffer cells. This study unveils the mechanism whereby arachidonic acid and ethanol increase TNFα production in Kupffer cells, thus contributing to alcoholic liver disease.

scholarly journals The Aryl Hydrocarbon Receptor Modulates Production of Cytokines and Reactive Oxygen Species and Development of Myocarditis during Trypanosoma cruzi Infection

2016 ◽  
Vol 84 (10) ◽  
pp. 3071-3082 ◽  
Author(s):  
Andréia Barroso ◽  
Melisa Gualdrón-López ◽  
Lísia Esper ◽  
Fátima Brant ◽  
Ronan R. S. Araújo ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Trypanosoma Cruzi ◽  
Aryl Hydrocarbon Receptor ◽  
Reactive Oxygen ◽  
T Cell Subsets ◽  
Cytokine Signaling ◽  
Ros Production ◽  
Oxygen Species ◽  
Content Type ◽  
Aryl Hydrocarbon

The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor involved in controlling several aspects of immune responses, including the activation and differentiation of specific T cell subsets and antigen-presenting cells, thought to be relevant in the context of experimentalTrypanosoma cruziinfection. The relevance of AhR for the outcome ofT. cruziinfection is not known and was investigated here. We infected wild-type (WT) mice and AhR knockout (AhR KO) mice withT. cruzi(Y strain) and determined levels of parasitemia, myocardial inflammation and fibrosis, expression of AhR/cytokines/suppressor of cytokine signaling (SOCS) (spleen/heart), and production of nitric oxide (NO), reactive oxygen species (ROS), and peroxynitrite (ONOO−) (spleen). AhR expression was increased in the heart of infected WT mice. Infected AhR KO mice displayed significantly reduced parasitemia, inflammation, and fibrosis of the myocardium. This was associated with an anticipated increased immune response characterized by increased levels of inflammatory cytokines and reduced expression of SOCS2 and SOCS3 in the heart.In vitro, AhR deficiency caused impairment in parasite replication and decreased levels of ROS production. In conclusion, AhR influences the development of murine Chagas disease by modulating ROS production and regulating the expression of key physiological regulators of inflammation, SOCS1 to -3, associated with the production of cytokines during experimentalT. cruziinfection.

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