Inhibition of in vivo histamine metabolism in rats by foodborne and pharmacologic inhibitors of diamine oxidase, histamine N-methyltransferase, and monoamine oxidase.
When [14C]histamine was administered orally to rats, an average of 80% of the administered radioactivity was recovered in the urine at the end of 24 hr. About 10% of the total dose was excreted via the feces. Analysis of 4-hr urine samples found imidazoleacetic acid to be the predominant metabolite (60.6%), with N tau-methylimidazoleacetic acid (8.6%), N tau-methylhistamine (7.3%), and N-acetylhistamine (4.5%) to be the minor metabolites. Histamine metabolism was inhibited by simultaneous oral administration of aminoguanidine, isoniazid, quinacrine, cadaverine, putrescine, tyramine, and beta-phenylethylamine. The administration of inhibitors resulted in an increased amount of unmetabolized histamine and a decreased amount of metabolites reaching the urine. Pharmacologic inhibitors were found to be more potent and have a longer duration of action than foodborne ones. The inhibitors could potentiate food poisoning caused by histamine by inhibiting its metabolism.
D000284:Administration, Oral; D006631:Amine Oxidase (Copper-Containing) / Q000037:antagonists & inhibitors*; D000818:Animals; D002250:Carbon Radioisotopes / Q000652:urine; D002851:Chromatography, High Pressure Liquid; D003959:Diamines / Q000494:pharmacology* / Q000652:urine; D005260:Female; D005517:Foodborne Diseases; D006632:Histamine / Q000378:metabolism* / Q000652:urine; D007093:Imidazoles / Q000652:urine; D051381:Rats; D011919:Rats, Inbred Strains
D002250:Carbon Radioisotopes; D003959:Diamines; D007093:Imidazoles; D006632:Histamine; D006631:Amine Oxidase (Copper-Containing)