Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To assess functional activity of leukocytes, lipid peroxidation and enzymes indicating the severity of organ lesion in food poisoning and acute dysentery, the investigators employed the techniques of luminol- and biacridine-activated chemiluminescence of pure granulocyte population and whole blood, plasma chemiluminescence, assays of AAT, AsAT, AP, LDG. A relationship was established between chemiluminescence of leukocytes and whole blood, between leukocytic functional activity and the disease duration and severity. Indomethacin treatment of the patients reduced intoxication, did not affect leukocytic function, diminished plasma chemiluminescence. Functional activity of leukocytes and the enzymes levels were prognostically significant. Low response of leukocytes to the stimulus, i.e. a small rise of functional activity, served an unfavourable prognostic sign. A role of active oxygen forms produced by leukocytes is suggested in pathogenesis of alimentary toxo-infection.
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PMID:[Functional activity of leukocytes and enzyme indicators in acute intestinal infections]. 161 Dec 59

The present study examined the possible involvement of endogenous cyclooxygenase-derived factors in the lethality and hepatic hemorrhagic necrosis induced by phalloidin. Mice were pretreated with indomethacin, aspirin or ibuprofen (all inhibitors of cyclooxygenase) and injected with phalloidin (2 mg/kg). The toxin induced 75% lethality and caused severe hemorrhagic necrosis of the liver associated with increased serum levels of AST and ALT. Indomethacin completely prevented the mortality and hepatic damage elicited by phalloidin as judged by morphologic analysis and serum AST and ALT release. The in vitro addition of indomethacin to suspensions of freshly-isolated hepatocytes decreased plasma membrane bleb formation induced by phalloidin. In contrast to indomethacin, aspirin and ibuprofen did not influence phalloidin toxicity in vivo. These results suggest that inhibition of prostanoids per se may not be the sole mechanism of protection by indomethacin.
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PMID:Protection by indomethacin against the lethality and hepatotoxicity of phalloidin in mice. 816 Feb 14

The aim of our study was to evaluate the impact of impaired barrier function of the small intestine induced by indomethacin on biochemical markers of liver damage (serum levels of alanine aminotransferase, aspartate aminotransferase, bilirubin), and liver functional parameters (serum concentration of albumin, liver DNA synthesis). Indomethacin (Sigma) was administered in 2 injections in a dose of 7.5 mg/kg subcutaneously spaced 24 hours apart, rats were sacrificed 24, 48 or 72 hours after the second dose of indomethacin. Control rats received indomethacin vehicle (5% NaHCO3, pH 7.4, 1.0 ml/kg) in the same manner. Small intestine injury was approved by increased permeability (measured as a lactulose-mannitol index). Significant increase of small intestine DNA synthesis (estimated by incorporation of 3H thymidine) in indomethacin-treated rats 48 (p < 0.01) and 72 (p < 0.05) hours after the second dose of indomethacin documents induction of reparative process. All biochemical markers of liver injury were significantly decreased in indomethacin treated rats in all recorded intervals (p < 0.05). By contraries, serum concentration of albumin, which predicates about liver function, was in indomethacin-treated rats significantly decreased in all intervals (p < 0.01). To explain these contrarious results of indomethacin-induced impaired barrier function of the small intestine on the liver deserves further studies.
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PMID:Liver response to indomethacin-induced intestinal injury. 1214 6