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Glycoprotein, metabolism, enzymic

Passive transcellular transport across the intestinal epithelium involves three discrete steps (1) uptake across the apical membrane, (2) diffusion through the cytoplasm, and (3) efflux across the basolateral membrane. Occasionally, drug molecules without favorable physicochemical properties traverse the intestinal epithelium using endogenous membrane transporters.6-8 In addition, the intestinal mucosa, with its numerous drug-metabolizing enzymes and efflux transporters, such as P-glycoprotein (Pgp), functions as a biochemical barrier.9... [Pg.162]

Abstract. TPA and RA have significant effects on glycolipid and glycoprotein biosynthetic enzymes in several cultured cell systems. This suggests that these compounds as well as other "tumor promoters" will be useful in further studies on the regulation and control of glycoconjugate metabolism (metabolic perturbants). Butyrate, TPA and RA appear to exert their effects at different points in the cell cycle. These results could mean that tumor promotion, differentiation and virus infection occur at discrete points in the cell cycle. Membrane glycoconjugates may participate in these processes in a dynamic time-dependent way. [Pg.241]

The blood-brain barrier is a biochemical as well as a physical barrier. Brain endothelial cells create an enzymatic barrier composed of secreted proteases and nucleotidases, as well as intracellular metabolizing enzymes such as cytochrome P-450. Furthermore, y-glutamyl transpeptidase, alkaline phosphatase, and aromatic acid decarboxylase are more prevalent in cerebral microvessels than in nonneuronal capillaries. The efflux transporter P-glycoprotein and other extrusion pumps are present on the membrane surface of endothelial cells, juxtaposed toward the interior of the capillary. Furthermore, CNS endothelial cells display a net negative charge at the interior of the capillaries and at the basement membrane. This provides an additional selective mechanism by impeding passage of anionic molecules across the membrane. [Pg.761]

St John s wort can cause drug interactions by inducing hepatic microsomal drug-metabolizing enzymes or the drug transporter P-glycoprotein, which causes a net efflux of substrates, such as amitriptyline, from intestinal epithelial cells into the gut lumen (SEDA-24,12). In 12 patients (9 women, 3 men) the addition of St John s wort 900 mg/ day to amitriptyline 150 mg/day led to a 20% reduction in plasma amitriptyline concentrations, while nortriptyline concentrations were almost halved (210). [Pg.23]


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See also in sourсe #XX -- [ Pg.17 ]




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Metabolic enzymes

Metabolism enzymes

Metabolizing enzymes

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