The Experts below are selected from a list of 126 Experts worldwide ranked by ideXlab platform
Ortwin Brede - One of the best experts on this subject based on the ideXlab platform.
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Thiyl radicals in biosystems: inhibition of the Prostaglandin Metabolism by the cis-trans-isomerization of arachidonic acid double bonds.
Archives of biochemistry and biophysics, 2003Co-Authors: Susanne Kratzsch, K. Drössler, Helmut Sprinz, Ortwin BredeAbstract:This paper describes parallel and comparative experiments on the enzymatic cyclooxygenase (COX) driven conversion of arachidonic acid (AA, all-cis-5,8,11,14-eicosatetraenoic acid) into Prostaglandins by using pure arachidonic acid and AA samples containing relatively small amounts of thiyl radical induced trans-isomers. The experiments were performed in a liquid aqueous model system using COX-1 as well as by the in vitro feeding of VD(3)-differentiated and LPS-stimulated promyelocytic HL-60 cells using the cell's own COX-2. In the model solution, all the different test methods used (oxygen consumption, ROS induced luminescence, and TMPD oxidation) indicated the greatly disproportionate, non-stoichiometric inhibition of the Prostaglandin Metabolism by the trans-isomers. Accordingly, measurements performed in the cell system gave comparable results: both luminescence ROS detection and the ELISA test on PGE(2) expression resulted in the strong inhibition of the Prostaglandin Metabolism. We interpret these findings as enzyme blocking caused by just one mono-trans-isomerized double bond of AA.
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Thiyl radical-induced cis–trans-isomerization of arachidonic acid inhibits Prostaglandin Metabolism
Radiation Physics and Chemistry, 2003Co-Authors: Susanne Kratzsch, K. Drössler, Helmut Sprinz, Ortwin BredeAbstract:Abstract Thiyl radicals isomerize the olefinic bonds of natural all- cis- polyunsaturated fatty acids into their trans -state. Using low doses of gamma-irradiation we partially converted arachidonic acid (AA) by thiyl radical attack into its mono- trans -forms. The enzyme-driven Prostaglandin Metabolism was studied in these samples in liquid model as well as in in vivo conditions with four different detection methods. A dramatic inhibition of the Metabolism explained by blocking of the cyclooxygenase by trans-isomers has been found.
Susanne Kratzsch - One of the best experts on this subject based on the ideXlab platform.
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Thiyl radicals in biosystems: inhibition of the Prostaglandin Metabolism by the cis-trans-isomerization of arachidonic acid double bonds.
Archives of biochemistry and biophysics, 2003Co-Authors: Susanne Kratzsch, K. Drössler, Helmut Sprinz, Ortwin BredeAbstract:This paper describes parallel and comparative experiments on the enzymatic cyclooxygenase (COX) driven conversion of arachidonic acid (AA, all-cis-5,8,11,14-eicosatetraenoic acid) into Prostaglandins by using pure arachidonic acid and AA samples containing relatively small amounts of thiyl radical induced trans-isomers. The experiments were performed in a liquid aqueous model system using COX-1 as well as by the in vitro feeding of VD(3)-differentiated and LPS-stimulated promyelocytic HL-60 cells using the cell's own COX-2. In the model solution, all the different test methods used (oxygen consumption, ROS induced luminescence, and TMPD oxidation) indicated the greatly disproportionate, non-stoichiometric inhibition of the Prostaglandin Metabolism by the trans-isomers. Accordingly, measurements performed in the cell system gave comparable results: both luminescence ROS detection and the ELISA test on PGE(2) expression resulted in the strong inhibition of the Prostaglandin Metabolism. We interpret these findings as enzyme blocking caused by just one mono-trans-isomerized double bond of AA.
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Thiyl radical-induced cis–trans-isomerization of arachidonic acid inhibits Prostaglandin Metabolism
Radiation Physics and Chemistry, 2003Co-Authors: Susanne Kratzsch, K. Drössler, Helmut Sprinz, Ortwin BredeAbstract:Abstract Thiyl radicals isomerize the olefinic bonds of natural all- cis- polyunsaturated fatty acids into their trans -state. Using low doses of gamma-irradiation we partially converted arachidonic acid (AA) by thiyl radical attack into its mono- trans -forms. The enzyme-driven Prostaglandin Metabolism was studied in these samples in liquid model as well as in in vivo conditions with four different detection methods. A dramatic inhibition of the Metabolism explained by blocking of the cyclooxygenase by trans-isomers has been found.
Venugopal P. Menon - One of the best experts on this subject based on the ideXlab platform.
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Prostaglandin Metabolism during growth and differentiation of the regenerating vertebrate appendage
Prostaglandins leukotrienes and essential fatty acids, 1995Co-Authors: Appukuttan Jayadeep, Surapureddi Sailesh, Pallu Reddanna, U.n. Das, G. Ramesh, K. Vijay Kumar, Venugopal P. MenonAbstract:House lizards are able to regenerate their tails. This is an ideal model to study the growth and differentiation of an organ. Prostaglandins (PGs) are local hormones having diverse and potent biological activities. In an effort to understand PG Metabolism during the growth and differentiation of the regenerating lizard tail, we analysed the fatty acid (FA) composition of phospholipids are free FAs by GC, the activity of two rate-limiting enzymes (phospholipases A and C), the activity of the enzyme responsible for the oxygenation of polyunsaturated fatty acids to PGs (cyclooxygenase) and characterized the endogenous PGs by HPLC. It was observed that on the 20th day, i.e. the tissue differentiation period, there was an increase in phospholipase A activity, together with a sudden fall in the free arachidonic acid (AA) level, an increase in cyclooxygenase activity and the appearance of endogenous PGE2. PGE2 can stimulate cyclic adenosine monophosphate (cAMP) production and it may stimulate a cascade of events associated with tissue differentiation.
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Prostaglandin Metabolism during cell aggregation in the regenerating vertebrate appendage
Development Growth and Differentiation, 1993Co-Authors: Appukuttan Jayadeep, Surapureddi Sailesh, Pallu Reddanna, Venugopal P. MenonAbstract:Prostaglandin Metabolism during cell aggregation period was studied in the regenerating tail of the house lizard. On the basis of scanning electron microscopy it was observed that similar kinds of cells in the blastema aggregate to form promuscie aggregate and procartilage aggregate on the 13th day of tail regeneration. In order to understand the Prostaglandin Metabolism the following parameters were analysed. Fatty acid composition of phospholipids and free fatty acids analysed by gas chromatography. The activity of two rate limiting enzymes-phosholipase A and C, and the activity of the enzymes which are responsible for the oxygenation of polyunsaturated fatty acids-lipoxygenase and cycloxygenase were also estimated. The characterization of the endogenous Prostaglandins were carried out by high performance liquid chromatography. On the basis of the above investigations, we observed an increase in phospholipase C activity and resultant increase in free arachidonic acid level. High activity of cycloxygenase and presence of Prostaglandin E2 (PGE2) were also observed PGE2 was reported to stimulate cAMP production and resultant cell differentiation. These observations suggest the involvement of Prostaglandin Metabolism during cell aggregation period in the regenerating blastema and resultant cytodifferentiation of blastemal cells.
Mary L Williams - One of the best experts on this subject based on the ideXlab platform.
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peroxisomal abnormality in fibroblasts from involved skin of child syndrome case study and review of peroxisomal disorders in relation to skin disease
Archives of Dermatology, 1992Co-Authors: Soheyla Emami, William B Rizzo, Karen Hanley, Michael J Taylor, Marc E Goldyne, Mary L WilliamsAbstract:• Background and Design.— Peroxisomal deficiency has been described in a number of syndromes characterized by chondrodysplasia punctata, including the Conradi-Hunermann (C-H) syndrome. Because of overlapping clinical features of X-chromosome inheritance, ichthyosis, and limbreduction defects in C-H and CHILD (congenital hemidysplasia with ichthyosiform erythroderma and limb defects) syndromes, we examined peroxisomal content using diaminobenzidine cytochemistry and peroxisomal functions in fibroblasts from involved vs uninvolved skin of CHILD syndrome. Results.— Fibroblasts from involved skin of a patient with CHILD syndrome accumulated cytoplasmic lipid, visualized with the fluorescent probe, nile-red. Ultrastructurally, fibroblasts of involved skin of CHILD syndrome accumulated lamellated membrane and vacuolar structures. By diaminobenzidine ultracytochemistry, fewer peroxisomes were present. Moreover, the activities of two peroxisomal enzymes, catalase and dihydroxyacetone phosphate acyltransferase, were decreased (approximately 30% of normal). However, peroxisomal oxidation of very-long-chain and branched-chain fatty acids was preserved. Moreover, plasma very-long-chain fatty acids, plasma phytanic acid, and erythrocyte plasmalogen content were normal. Conclusions.— The CHILD, C-H, and rhizomelic chondrodysplasia punctata syndromes are all characterized by ichthyosis, chondrodysplasia punctata, and limb defects, as well as peroxisomal deficiency. Thus, these syndromes may be related pathogenically. Because peroxisomes are involved in Prostaglandin Metabolism, peroxisomal deficiency may directly contribute to the previously reported alterations in Prostaglandin Metabolism in fibroblasts of involved skin of fibroblasts. ( Arch Dermatol. 1992;128:1213-1222)
D Zaremba-drobnik - One of the best experts on this subject based on the ideXlab platform.
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Platelet aggregation and Prostaglandin Metabolism in uremic patients.
American journal of kidney diseases : the official journal of the National Kidney Foundation, 2001Co-Authors: I Pietrzak, M Komarnicki, D Zaremba-drobnikAbstract:The pathogenesis of depressed platelet activity in uremia is still unknown. The influence of some uremic toxins on platelet aggregation (PLA) and Prostaglandin Metabolism in 50 uremic patients treated by hemodialysis (HD) or continuous ambulatory peritoneal dialysis (CAPD) was studied. Fifty-seven healthy volunteers (HVs) served for reference values. Adenosine diphosphate (ADP) and thrombin (Thr) were used as agonists of PLA. PLA was determined using the Born method. Malonyldialdehyde (MDA) levels in platelets as an indicator of Prostaglandin Metabolism, after stimulation with arachidonic acid, were measured according to Stuart. The relationship of PLA and Prostaglandin Metabolism with plasma concentrations of methylguanidine (MG), guanidinosuccinic acid (GSA), and creatinine (Cr) was assessed. PLA-ADP values in regular HD patients (42 +/- 5 mm) were significantly lower than in CAPD patients (65 +/- 8 mm) and HVs (73 +/- 3 mm). PLA-Thr values in HD patients (25 +/- 4 mm) were significantly lower than in CAPD patients (34.9 mm) and HVs (36 +/- 3 mm). MDA levels in HD patients (7 +/- 1 nmol/L/10(9)) were significantly lower than in CAPD patients (12 +/- 2 nmol/L/10(9)) and HVs (15 +/- 1 nmol/L/10(9)). In HD patients, inverse correlations of PLA-ADP with MG levels (r = -0.92), PLA-Thr with Cr levels (r = -89), and MDA levels with GSA levels (r = -0.86) were found. In CAPD patients, no relationship of PLA and MDA with uremic toxins was observed. Depressed activity of platelets and Prostaglandin Metabolism was strongly expressed in HD patients.
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Platelet aggregation and Prostaglandin Metabolism in uremic patients.
American Journal of Kidney Diseases, 2001Co-Authors: I Pietrzak, M Komarnicki, D Zaremba-drobnikAbstract:Abstract The pathogenesis of depressed platelet activity in uremia is still unknown. The influence of some uremic toxins on platelet aggregation (PLA) and Prostaglandin Metabolism in 50 uremic patients treated by hemodialysis (HD) or continuous ambulatory peritoneal dialysis (CAPD) was studied. Fifty-seven healthy volunteers (HVs) served for reference values. Adenosine diphosphate (ADP) and thrombin (Thr) were used as agonists of PLA. PLA was determined using the Born method. Malonyldialdehyde (MDA) levels in platelets as an indicator of Prostaglandin Metabolism, after stimulation with arachidonic acid, were measured according to Stuart. The relationship of PLA and Prostaglandin Metabolism with plasma concentrations of methylguanidine (MG), guanidinosuccinic acid (GSA), and creatinine (Cr) was assessed. PLA-ADP values in regular HD patients (42 ± 5 mm) were significantly lower than in CAPD patients (65 ± 8 mm) and HVs (73 ± 3 mm). PLA-Thr values in HD patients (25 ± 4 mm) were significantly lower than in CAPD patients (34.9 mm) and HVs (36 ± 3 mm). MDA levels in HD patients (7 ± 1 nmol/L/109) were significantly lower than in CAPD patients (12 ± 2 nmol/L/109) and HVs (15 ± 1 nmol/L/109). In HD patients, inverse correlations of PLA-ADP with MG levels (r = −0.92), PLA-Thr with Cr levels (r = −89), and MDA levels with GSA levels (r = −0.86) were found. In CAPD patients, no relationship of PLA and MDA with uremic toxins was observed. Depressed activity of platelets and Prostaglandin Metabolism was strongly expressed in HD patients. © 2001 by the National Kidney Foundation, Inc.
