COX1Cytochrome Oxidase Subunit 1
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09 15460 16599 1,140 4 tRNA Thr -- 16600 16667 68 0 tRNA Pro -- 16667 16731 65 -1 (1) bp, base pairs; (2) tRNA, transfer RNA and italic words are replaced by one amino acid code; (3) rRNA, ribosomal RNA; 4) 12S rRNA, small rRNA subunit; (5) 16S rRNA, large rRNA subunit; (6) ND1-6 and ND4l, genes encoding nicotinamide adenine dinucleotide dehydrogenase subunits 1 to 6 and 4l; (7) COX1 to 3, genes encoding cytochrome c oxidase subunits I to III; (8) T--, incomplete termination codon; (9) ATPase6 and 8, genes encoding adenosine triphosphatase subunits 6 and 8; (10) Cytb, gene encoding cytochrome b.
Key words: amphibian, Anuran, COX1 gene, genetic analysis, Plains Spadefoot, Spea bombifrons, species identification, Wyoming, Yellowstone National Park
However, it is reasonable to assume that the cardiovascular risk of these drugs will be associated with the degree and duration of inhibition of COX2 and that the ratio between COX1 and COX2 will be determinant in their relative tendency to cause this side effect (29,30).
Neither meloxicam nor celecoxib affected clotting times in canines compared with reports from other authors that found a COX1 inhibitor as an inhibiting factor of platelet aggregation or thrombotic action of celecoxib.
Genetic polymorphism of enzymes like COX1,COX-2 or thromboxane A2 synthase,
Inhibit important enzyme systems such as 5-LOX and COX1 that produce inflammatory mediators called leukotrienes and prostaglandins.
In one study by Brida et al on NSAIDs drugs, indicated that Flunixin meglumine have a high inhibitory effect on COX1, this result in one study by Brita were corroborated [4,8].
Aspirin is a very effective antiinflammatory drug because it covalently and irreversibly modifies COX1 and COX2, thereby blocking the rate-limiting step of prostaglandin synthesis.
Green tea constituent epigallocatechin-3-gallate selectively inhibits COX-2 without affecting COX1 expression in human prostate carcinoma cells.
The toxicity of NSAIDs is related to the COX1 inhibition of prostaglandin synthesis.
The trouble is, these pathways do some good too and it is important to inhibit COX2 without affecting COX1 too much.
El hecho de que los inhibidores de la COX1 y de la COX2 no hayan disminuido significativamente la produccion de PGE2 pero si hayan prevenido la inflamacion (evaluada histologicamente y como actividad MPO en vejiga) parece indicar que otras prostaglandinas diferentes a la PGE2 u otros mecanismos mediados por COX podrian tener un papel relevante en este modelo de cistitis.