No description available.

Seventeen wk old male obese Zucker rats were given 0.4% (w/w) conjugated linoleic acid (CLA) isomers for 8 wk to determine effects of specific isomers on multiple eicosanoids in obesity. Liquid-chromatography-mass spectrometry analysis showed that compared to controls, those given t10,c12 CLA had increased liver leukotriene B4 levels, while immunoblotting revealed that rats given either t10,c12 or c9,t11 CLA had lower liver cyclooxygenase-2. In kidney, compared to c9,t11 CLA or controls, t10,c12 CLA increased cyclooxygenase-1, 6-keto-prostaglandin F2α and thromboxane B2 and inhibited the in vitro production of 13-hydroxyoctadecadienoic acid and 5-, 8-, 12- and 15-hydroxyeicosatetraenoic acid. In lean compared to fa/fa rats, endogenous levels and in vitro production of liver and kidney 9- and 13-hydroxyoctadecadienoic acid were elevated. Previous investigations on these tissues revealed that t10,c12 CLA reduced hepatic steatosis, but increased renal damage. How these changes in eicosanoids in response to t10,c12 CLA relate to the previous findings remains to be elucidated.

Seventeen wk old male obese Zucker rats were given 0.4% (w/w) conjugated linoleic acid (CLA) isomers for 8 wk to determine effects of specific isomers on multiple eicosanoids in obesity. Liquid-chromatography-mass spectrometry analysis showed that compared to controls, those given t10,c12 CLA had increased liver leukotriene B4 levels, while immunoblotting revealed that rats given either t10,c12 or c9,t11 CLA had lower liver cyclooxygenase-2. In kidney, compared to c9,t11 CLA or controls, t10,c12 CLA increased cyclooxygenase-1, 6-keto-prostaglandin F2α and thromboxane B2 and inhibited the in vitro production of 13-hydroxyoctadecadienoic acid and 5-, 8-, 12- and 15-hydroxyeicosatetraenoic acid. In lean compared to fa/fa rats, endogenous levels and in vitro production of liver and kidney 9- and 13-hydroxyoctadecadienoic acid were elevated. Previous investigations on these tissues revealed that t10,c12 CLA reduced hepatic steatosis, but increased renal damage. How these changes in eicosanoids in response to t10,c12 CLA relate to the previous findings remains to be elucidated.

No description available.

Thesis (M.S.)--West Virginia University, 2005. / Title from document title page. Document formatted into pages; contains vii, 82 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 60-82).

No / High personal UVR doses can be gained during leisure activities, causing intense self-resolving inflammation (sunburn) of unprotected skin. UVR activates release of membrane fatty acids and upregulates their metabolism by cyclooxygenases (COX) and lipoxygenases (LOX) to different eicosanoids. While COX-derived prostaglandin (PG)E2 is a potent mediator of sunburn vasodilatation, LOX-derived 15-hydroxyeicosatetraenoic acid (HETE) and its lipoxin metabolites may contribute to sunburn limitation. We explored the relationships between expression of these lipid mediators and the clinical and histological outcomes, comparing responses of individuals prone and more resistant to sunburn. An acute UVR exposure of 12 SED (standard erythema dose) was applied to buttock skin of 32 white Caucasians (n = 16 phototype I/II, n = 16 phototype III/IV), and over the subsequent 72 h assessments were made of skin erythema, immunohistochemical expression of leukocyte markers, COX-2, 12-LOX, 15-LOX and nitric oxide synthase (NOS), and eicosanoid levels by LC/ESI-MS/MS. Evidence of a significant inflammatory response was seen earlier in phototype I/II with regard to expression of erythema (4h, p < 0.001), neutrophil infiltration (24 h, p = 0.01), epidermal COX-2 (24 h, p < 0.05) and 12-LOX (24 h, p < 0.01), and dermal eNOS (24 h, p < 0.05) proteins, although CD3+ lymphocyte infiltration showed an earlier increase in phototype III/IV (24 h, p < 0.05). Although erythema was equivalent at 72 h in both groups, phototype I/II showed higher PGE2 accompanied by elevated 15-HETE, and a strong positive correlation was seen between these mediators (n = 18, r = 0.805, p = 0.0001). Hence anti-inflammatory eicosanoid 15-HETE may temper the pro-inflammatory milieu in sunburn, having greater influence in those prone to sunburn than those more resistant, given the same high UVR exposure conditions. / The Wellcome Trust

Placental dysfunction is implicated in the pathogenesis of preeclampsia. Chemical signals between the placenta and maternal circulation are a suspect cause of endothelial dysfunction and maternal hypertension. This study examined select lipid mediators of inflammation produced by the placenta. Patients were recruited from Virginia Commonwealth University’s pregnancy clinics and placentas were collected at delivery. Forty-eight-hour explant cultures of villous placental tissue were used to model lipid production. Electrospray ionization mass spectrometry was used to quantify concentrations of free lipids in the culture media. Bicinchoninic acid assays were performed to quantify protein in each culture for normalization of lipid data. After analysis, it was found that severity of preeclampsia was correlated with a unique lipid profile. Pro-inflammatory hydroxyeicosatetraenoic acids and sphingolipids were elevated. Aspirin usage in patients who developed preeclampsia was found to attenuate accumulation of isoprostane oxidative stress markers and thromboxane production while preserving omega-3-fatty acid and increasing prostacyclin levels.

Thesis (Ph. D.)--University of Missouri--Columbia, 2002. / "May 2002." Typescript. Includes bibliographical references. Also available on the Internet.

Thesis (Ph. D.)--Ohio State University, 2007. / Title from first page of PDF file. Includes bibliographical references (p. 178-204).

Owing at least in part to oxysterol components that can induce apoptosis, oxidized LDL (oxLDL) is cytotoxic to mammalian cells with receptors that can internalize it. Vascular cells possess such receptors, and it appears that the apoptotic response of vascular cells to the oxysterols borne by oxLDL is an important part of the atherogenic effects of oxLDL. Thus, an analysis of the signaling pathway of apoptotic induction by oxysterols is of value in understanding the development of atherosclerotic plaque. In a prior study, we demonstrated an induction of calcium ion flux into cells treated with 25-hydroxycholesterol (25-OHC) and showed that this response is essential for 25-OHC-induced apoptosis. One possible signal transduction pathway initiated by calcium ion fluxes is the activation of cytosolic phospholipase A2 (cPLA2). In the current study, we demonstrate that activation of cPLA2 does occur in both macrophages and fibroblasts treated with 25-OHC or oxLDL. Activation is evidenced by 25-OHC-induced relocalization of cPLA2 to the nuclear envelope and arachidonic acid release. Loss of cPLA2 activity, either through genetic knockout in mice, or by treatment with a cPLA2 inhibitor, results in an attenuation of arachidonic acid release as well as of the apoptotic response to oxLDL in peritoneal macrophages or to 25-OHC in cultured fibroblast and macrophage cell lines.