By A. F. Rowley, Hartmut Kühn, T. Schewe
Eicosanoids are a various workforce of biologically energetic molecules derived from polyunsaturated fatty acid precursors. This quantity attracts jointly for the 1st time a chain of overviews at the biosynthesis and practical value of those and similar compounds in quite a lot of animals, crops, and micro-organisms. All chapters are written via famous specialists of their fields, and plenty of utilize a great deal of unpublished fabrics. This quantity is geared toward complicated undergraduates and at researchers attracted to lipid biochemistry and normal plant and animal biology.
Originally released in 1999.
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Therefore, selective inhibition of C O X -2 activity w ould provide a significant im provem ent over therapeutics fo r inflam m atory diseases. Several arom atic com pounds w ith a m ethyl sulph o n y l group, such as N S-398, N imesulide, T-614, FK3311, Floslide, L-745337, D up-697 and SC-58125 have been developed as C O X -2-specific inhibitors . R ecent studies have identified N S A ID s th a t preferentially inhibit C O X -I o r C O X -2 , o r in h ib it b o th isoform s equally [17-19], T he different affinities tow ard som e fatty acid substrates and N S A ID s suggested a subtle difference betw een the active sites of C O X -I and C O X -2.
T he observation suggests th a t C O X -I and C O X -2 in the E R and C O X -2 in the N E constitute independent prostanoid biosynthetic systems. M ost of the current know ledge on the biological contributions of the tw o C O X isoform s has come from studies by N SA ID inhibition, C O X -2 induction or both. Both gene d isruption and overexpression of the C O X isoform s have recently been developed as alternative approaches to investigate the problem . It has been dem onstrated th at C O X -I gene d isru p tio n reduces arachidonic acid-induced inflam m ation and indom ethacin-induced gastric ulceration in mice , O n the o th er hand, renal abnorm alities and an altered inflam m atory response w ere observed in mice w ith C O X -2 gene disruption [26,27], Rat intestinal epithelial cells p erm anently infected w ith a C O X -2 expression vector show ed n o t o nly the elevated expression level of C O X -2 p rotein, b u t also b o th increased adhesion to extracellular matrix and inhibition of apoptosis .
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