Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.108 (lactase)
 2,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study the influence of 14 antibiotics, 12 of them orally applicable, on human enterokinase was investigated. The effects of these substances on the activities of human disaccharidases were also examined. The enterokinase activity is more sensitive to the studied antibiotics than is human lactase, saccharase or isomaltase. Unphysiologically high concentrations of penicillins, cephalexin and chloramphenicol (10(-2) Mol/l) inhibited enterokinase, tetracycline (doxycycline) in a dose of 10(-3) m reduced the activity of this enzyme by 50%, neomycinsulphate and the sulphates of polymyxin B and E have no effect on the disaccharidases. On the contrary, these substances are the best inhibitors of enterokinase among the tested antibiotics. Neomycin or polymyxin (10(-4) Mol/l) causes a 50% inhibition of a physiological quantity of this enzyme. Therapeutic doses of both antibiotics may reduce the enterokinase activity by 70% to 90%, while the activity of trypsin is not affected unless a concentration greater than 10(-2) m is used. The inhibition is not only caused by the anion (SO4) of these antibiotics, since sulphates reduce the enterokinase only in concentrations higher than 10(-3) Mol/l in man. The mechanism of inhibition is not effected by binding cholic acids under test conditions. Both polymyxin and neomycin inhibit the enterokinase activity with and without glycodeoxycholic acid. Further studies showed that the type of inhibition is competitive in both cases. The inhibition constant K2 of neomycin-B-sulphate is 8.7X10(-5) Mol/l, of polymyxin-E-sulphate 8.6X10(-5) Mol/l. The inhibition type of penicillins, cephalosporins and doxycycline is noncompetitive, thus contrasting that of neomycin and polymyxin.
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PMID:[The influence of orally applicable antibiotics on the activities of human enterokinase and disaccharidases (author's transl)]. 98 20

Lactose intolerance occurs in the majority of human groups, excluding people from Northern Europe. Because its effect is similar to that of lactulose, lactose seems to be an alternative treatment for patients with portal-systemic encephalopathy (PSE) and lactase deficiency. The mechanism of action of lactose is similar to that of lactulose. In vivo, lactose improves PSE parameters and causes acidic diarrhea. We performed in vitro studies in a fecal incubation system to investigate the biochemical and bacteriological effects induced by different substances customarily used for the treatment of patients with PSE (lactose, lactulose and Neomycin). In vitro experiments showed that lactose and lactulose decreased aerobic flora counts and reduced the pH of fecal incubation. Both disaccharides reduced the ammonia concentration in the incubation system.
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PMID:In vitro and in vivo lactose and lactulose effects on colonic fermentation and portal-systemic encephalopathy parameters. 914 47