By V. Ullrich, M. Hecker, R. Nüsing, T. Rosenbach (auth.), Santosh K. Nigam Ph.D., M.B., B.Ch., David C. H. McBrien Ph.D., Trevor F. Slater Ph.D., D.Sc., M.D.(Hon.) (eds.)
This quantity provide you with updated, specialist reports of this fast-moving field.The major themes are in line with the interrelationships among arachidonate metabolism, platelet-activating issue, lipid peroxidation and melanoma. The reports offer very important details for the professional and also will be of worth to a large viewers attracted to advancements in cellphone biology, pharmacology, pathology, biochemistry and melanoma.
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Additional resources for Eicosanoids, Lipid Peroxidation and Cancer
The effeet ofTPAon tumour cell adhesion was also reduced by LOX inhibitors (data not shown). These results suggest to us that TPA by a LOX dependent mechanism may increase surface expression of IRGPIIb/lIIa receptors and/or "aetivate" existing IRGPIIb/I1la receptors. To test this hypothesis, MS751 cells were stimulated with 12-HETE or TPA in the presence of a LOX inhibitor (i. , quercetin) at concentrations which did not inhibit protein kinase C. Following stimulation the cells were labelIed with a specific monoclonal antibody to GPIIb/I1la, followed by a secondary antibody conjugated to fluorescein and quantitated by flow cytometric analysis.
Table 2. 001 Table 3. OOl 46 S. K. Nigam and R. Averdunk An increase in eicosanoid levels in the plasma was found as early as 2 h after the inoculation of tumour cells. It decreased slightly within the first 3 days for lymphoma cells and 1 day for CAM cells and then again increased markedly (Table 3). Plasma concentrations of eicosanoids correlated well with the number of cells inoculated and the duration of tumour growth. From the above data it is evident that TXA z is the principal arachidonic acid metabolite in the circulation of rats and is possibly a potent inducer of tumour growth.
Mehta and coworkers (1983, 1984) determined in vitro that the PGI 2 biosynthetic capability of vessels removed from patients with osteogenic sarcoma was less than that of vessels removed from patients without cancer. 1. Effect of TXSI (CGS 14854) and LOX (quercetin) inhibitors on Walker 256 carcinosarcoma-induced platelet aggregation. Aggregation of homologous plateletrich plasma was induced by 5 x 105 tumour cells. c g> 20 CGS14854 + QUERCETIN 10 O~---T/-d~------·5 o 5 10 15 time (min) normal controls.
Eicosanoids, Lipid Peroxidation and Cancer by V. Ullrich, M. Hecker, R. Nüsing, T. Rosenbach (auth.), Santosh K. Nigam Ph.D., M.B., B.Ch., David C. H. McBrien Ph.D., Trevor F. Slater Ph.D., D.Sc., M.D.(Hon.) (eds.)