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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Comparative irritancy of oxaprozin on the gastrointestinal tract of rats and mice: relationship to drug uptake and effects in vivo on eicosanoid metabolism.

Studies were performed in rats and mice to investigate the mechanisms of the comparatively low irritancy in the gastrointestinal (GI) tract of oxaprozin, relative to that of other non-steroidal anti-inflammatory drugs. A single dose of oxaprozin (100 mg/kg), given orally to rats, reduced the concentration of prostaglandin E2, but did not produce any gastric lesions or mucosal irritation, either visibly or when the mucosa was examined by scanning or transmission electronmicroscopy. The low gastric irritancy was reflected by lower concentrations of the drug in the gastric mucosa, compared with those in the upper intestinal tract, following oral administration of 100 mg/kg of [14C]oxaprozin. This distribution of the drug in the gastrointestinal tract reflected the absence of gastric irritancy when the drug was given repeatedly for 5 days by the oral route to rats. It was only after intraperitoneal administration of high doses of the drug that intestinal ulcers and peritonitis became evident, and then no gastric irritancy was observed. As with other non-steroidal anti-inflammatory drugs, there was some, but appreciably less, enhancement of gastric irritancy observed when the drug was given to mice treated with the cholinomimetic, bethanechol chloride (to enhance secretion of acid and pepsin). It is suggested that the inhibition of mucosal prostaglandin production by oxaprozin may be considered a 'priming' reaction, and that subsequent enhancement of irritancy occurs by stimulation of acid and pepsin. Structure--activity relationships of oxaprozin analogues were studied. The addition of electron-withdrawing substituents, which markedly enhance the gastric ulcerogenic effects of other non-steroidal anti-inflammatory drugs, only slightly enhanced the irritancy of oxaprozin, thus providing further evidence for the inherent low ulcerogenicity of this molecule.[1]

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