scholarly journals Mitochondrial P450-dependent arachidonic acid metabolism by TCDD-induced hepatic CYP1A5; conversion of EETs to DHETs by mitochondrial soluble epoxide hydrolase

2007 ◽  
Vol 468 (1) ◽  
pp. 70-81 ◽  
Author(s):  
Erin M. Labitzke ◽  
Silvia Diani-Moore ◽  
Arleen B. Rifkind
Keyword(s):  
Arachidonic Acid ◽  
Epoxide Hydrolase ◽  
Acid Metabolism ◽  
Soluble Epoxide Hydrolase ◽  
Arachidonic Acid Metabolism

Acute arsenic toxicity alters cytochrome P450 and soluble epoxide hydrolase and their associated arachidonic acid metabolism in C57Bl/6 mouse heart

Xenobiotica ◽  
2012 ◽  
Vol 42 (12) ◽  
pp. 1235-1247 ◽  
Author(s):  
Anwar Anwar-Mohamed ◽  
Ahmed A. El-Sherbeni ◽  
Seok H. Kim ◽  
Hassan N. Althurwi ◽  
Beshay N. M. Zordoky ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Cytochrome P450 ◽  
Epoxide Hydrolase ◽  
Acid Metabolism ◽  
Soluble Epoxide Hydrolase ◽  
Arachidonic Acid Metabolism ◽  
Mouse Heart ◽  
Arsenic Toxicity

scholarly journals Modulation of Arachidonic Acid Metabolism in the Rat Kidney by Sulforaphane: Implications for Regulation of Blood Pressure

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Fawzy Elbarbry ◽  
Anke Vermehren-Schmaedick ◽  
Agnieszka Balkowiec
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Arachidonic Acid ◽  
Epoxide Hydrolase ◽  
Rat Kidney ◽  
Soluble Epoxide Hydrolase ◽  
Arachidonic Acid Metabolism ◽  
Dependent Manner ◽  
Shr Rats ◽  
Arterial Blood

Background. We investigated the effects of sulforaphane (SF), the main active isothiocyanate in cruciferous vegetables, on arachidonic acid (AA) metabolism in the kidney and its effect on arterial blood pressure, using spontaneously hypertensive rats (SHR) as models. Methods. Rats were treated for 8 weeks with either drinking water alone (control) or SF (20 or 40 mg/kg) added to drinking water. Mean arterial pressure (MAP) was measured at 7-day intervals throughout the study. At the end of treatment rats were euthanized, and kidneys were harvested to prepare microsomes and measure enzymes involved in regulation of vasoactive metabolites: CYP4A, the key enzyme in the formation of 20-hydroxyeicosatetraenoic acid, and the soluble epoxide hydrolase, which is responsible for the degradation of the vasodilator metabolites such as epoxyeicosatetraenoic acids. Effect of SF on kidney expression of CYP4A was investigated by immunoblotting. Results. We found that treatment with SF leads to significant reductions in both, the expression and activity of renal CYP4A isozymes, as well as the activity of soluble epoxide hydrolase (sEH). Consistent with these data, we have found that treatment with SF resisted the progressive rise in MAP in the developing SHR in a dose-dependent manner. Conclusion. This is the first demonstration that SF modulates the metabolism of AA by both P450 enzymes and sEH in SHR rats. This may represent a novel mechanism by which SF protects SHR rats against the progressive rise in blood pressure.

Regulation of arachidonic acid metabolism in human amnion

1985 ◽  
Vol 110 (1_Suppla) ◽  
pp. S53-S54
Author(s):  
ST. NIESERT ◽  
M. D. MITCHELL ◽  
M. L. CASEY ◽  
P. C. MACDONALD
Keyword(s):  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Human Amnion

Arachidonic acid metabolism and insulin secretion by isolated human pancreatic islets

Diabetes ◽  
1988 ◽  
Vol 37 (7) ◽  
pp. 992-996 ◽  
Author(s):  
J. Turk ◽  
J. H. Hughes ◽  
R. A. Easom ◽  
B. A. Wolf ◽  
D. W. Scharp ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Human Pancreatic Islets

The interaction Between Arachidonic Acid Metabolism and Homocysteine

2020 ◽  
Vol 20 ◽  
Author(s):  
Elisa Domi ◽  
Malvina Hoxha ◽  
Bianka Hoxha ◽  
Bruno Zappacosta
Keyword(s):  
Cardiovascular Disease ◽  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Neurological Diseases ◽  
Arachidonic Acid Metabolism ◽  
Epoxyeicosatrienoic Acids ◽  
Pathological Conditions ◽  
Literature Searches ◽  
Hydroxyeicosatetraenoic Acids ◽  
Improve Health

Purpose: Hyperhomocysteinemia (HHcy) has been considered a risk factor for different diseases including cardiovascular disease (CVD), inflammation, neurological diseases, cancer and many other pathological conditions. Likewise, arachidonic acid (AA) metabolism is implicated in both vascular homeostasis and inflammation as shown by the development of CVD following the imbalance of its metabolites. Aim of The Review: This review summarizes how homocysteine (Hcy) can influence the metabolism of AA. Methods: In silico literature searches were performed on PubMed and Scopus as main sources. Results: Several studies have shown that altered levels of Hcy, through AA release and metabolism, can influence the synthesis and the activity of prostaglandins (PGs), prostacyclin (PGI₂), thromboxane (TXA), epoxyeicosatrienoic acids (EETs) and hydroxyeicosatetraenoic acids (HETEs). Conclusions: We believe that by targeting Hcy in AA pathways, novel compounds with better pharmacological and pharmacodynamics benefits may be obtained and that this information is valuable for dietician to manipulate diets to improve health.

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