Prostaglandins, leukotrienes, and essential fatty acids
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Prostaglandins Leukot. Essent. Fatty Acids · Jan 2001
Effects of essential fatty acid deficiency and supplementation with docosahexaenoic acid (DHA; 22:6n-3) on cellular fatty acid compositions and fatty acyl desaturation in a cell culture model.
The desaturation of [1-(14)C] 18:3n-3 to docosahexaenoic acid (DHA; 22:6n-3) is enhanced in an essential fatty acid deficient cell line (EPC-EFAD) in comparison with the parent cell line (EPC) from carp. In the present study, the effects of DHA on lipid and fatty acid compositions, and the metabolism of [1-(14)C]18:3n-3 were investigated in EPC-EFAD cells in comparison with EPC cells. DHA supplementation had only relatively minor effects on lipid content and lipid class compositions in both EPC and EPC-EFAD cells, but significantly increased the amount of DHA, 22:5n-3, eicosapentaenoic acid (EPA; 20:5n-3), total n-3 polyunsaturated fatty acids (PUFA), total PUFA and saturated fatty acids in total lipid and total polar lipid in both cell lines. ⋯ Consistent with this, the suppression of DHA production upon DHA supplementation was associated with increased cellular and membrane DHA concentrations in EPC-EFAD cells. However, an increase in cellular DHA content to similar levels failed to suppress DHA production in DHA-supplemented EPC cells. A possible explanation is that greatly increased levels of EPA, derived from retroconversion of the added DHA, acts to offset the suppression of the pathway by DHA by stimulating conversion of EPA to DHA in DHA-supplemented EPC cells.
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Prostaglandins Leukot. Essent. Fatty Acids · Dec 2000
ReviewBeneficial effect(s) of n-3 fatty acids in cardiovascular diseases: but, why and how?
Low rates of coronary heart disease was found in Greenland Eskimos and Japanese who are exposed to a diet rich in fish oil. Suggested mechanisms for this cardio-protective effect focused on the effects of n-3 fatty acids on eicosanoid metabolism, inflammation, beta oxidation, endothelial dysfunction, cytokine growth factors, and gene expression of adhesion molecules; But, none of these mechanisms could adequately explain the beneficial actions of n-3 fatty acids. One attractive suggestion is a direct cardiac effect of n-3 fatty acids on arrhythmogenesis. ⋯ Based on this, it is suggested that the principle mechanism of cardioprotective and neuroprotective action(s) of n-3 fatty acids can be due to the suppression of TNFalpha and IL synthesis and release, modulation of hypothalamic-pituitary-adrenal anti-inflammatory responses, and an increase in acetylcholine release, the vagal neurotransmitter. Thus, there appears to be a close interaction between the central nervous system, endocrine organs, cytokines, exercise, and dietary n-3 fatty acids. This may explain why these fatty acids could be of benefit in the management of conditions such as septicemia and septic shock, Alzheimer's disease, Parkinson's disease, inflammatory bowel diseases, diabetes mellitus, essential hypertension and atherosclerosis.
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Prostaglandins Leukot. Essent. Fatty Acids · Apr 1998
Radioimmunoassay of 8-iso-prostaglandin F2alpha: an index for oxidative injury via free radical catalysed lipid peroxidation.
8-iso-prostaglandin F2alpha (8-iso-PGF2alpha), a major F2-isoprostane, is biosynthesized in vivo through nonenzymatic free radical-catalysed peroxidation of arachidonic acid. The levels of F2-isoprostanes both free in the circulation and esterified to the tissue phospholipids increase intensely in animal models of oxidant injury. This study presents the development and validation of a radioimmunoassay of 8-iso-PGF2alpha for the measurement of this substance in the body fluids. ⋯ Free 8-iso-PGF2alpha levels in plasma and urine from normal human volunteers are evaluated and found to correlate with the obtained values by gas chromatography-mass spectrometry methods from other studies. The levels of free 8-iso-PGF2alpha in the plasma and urine increased 7- and 102-fold, respectively, after CCl4 administration to rats. Thus, this 8-iso PGF2alpha radioimmunoassay method is relevant to apply in the oxidative injury studies as an index of in vivo lipid peroxidation through free radical catalysis mechanism.
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Prostaglandins Leukot. Essent. Fatty Acids · Feb 1996
Evaluation of the effects of steroids on experimental septic lung injury.
To evaluate the clinical usefulness of steroids for septic lung injury, we investigated the effects of methylprednisolone (MP) on this disorder using an experimental rat model of cecal ligation and puncture (CLP). While 92% of the rats that underwent CLP (CLP rats) died within 30 h, those given high-dose MP (30 mg/kg) just after the operation (CLP + MP rats) survived for a significantly longer period (p < 0.01). Concentrations of endotoxin (ET) in arterial blood were significantly higher in the CLP + MP rats than in the CLP rats, while those in the bronchoalveolar lavage fluid (BALF) were significantly lower. ⋯ The administration of MP did not cause recoveries in the uptake and release of 3H-AA by CLP-AM. Although the survival time of CLP rats was significantly prolonged and the translocation of ET into BALF was reduced by steroid administration, the steroid effects were not explained by those on altered AM function. The upregulated generation of O2- and reduced LTB4 production from CLP-AM were not reversed by the treatment of this drug.
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Prostaglandins Leukot. Essent. Fatty Acids · Aug 1993
Randomized Controlled Trial Clinical TrialThe effect of prostaglandin E1 on renal function after cardiac surgery involving cardiopulmonary bypass.
This study was performed to evaluate the effect of prostaglandin E1 (PGE1) on renal function after cardiac surgery in patients undergoing cardiopulmonary bypass (CPB). Haemodynamic and renal functional response to low dose PGE1 (0.02 microgram kg-1 min-1) (group A) or saline (group B) infusion via peripheral vein during CPB was evaluated in 20 patients who underwent cardiac surgery. The perfusion pressure was maintained at about 60 mmHg during CPB in both groups. ⋯ Cardiac output (co) did not change in either group throughout this study. Pulmonary capillary wedge pressure (PCWP) in group A decreased significantly at 30 and 60 min after CPB, but in group B did not change throughout the study. Cardiac index (CI) decreased significantly at 60 min after CPB in group A (P < 0.05) and at 30 min in group B (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)