ABSTRACT
After injection of an intravenous bolus of heparin (15,000 IU) in two groups of subjects, 10 normal volunteers and 6 subjects with external biliary drainage, blood and urine samples were collected; in the latter group bile samples were collected also. All samples were assayed for diamine oxidase (DAO). Persistently high values of this enzyme were found in plasma of both populations after heparin stimulation, while no increase in enzymatic activity was detected in bile and urine. In order to confirm and support the hepatic clearance of DAO, liver uptake of the enzyme derived from porcine kidney, human plasma and human placenta was studied by perfusion of isolated rat liver. Disappearance curves of the enzyme derived from three different sources showed a prompt liver uptake: activity decreased by about 50% in 10 min (endocytic uptake) and a slower but constant reduction during the remaining 110 min of perfusion was observed. These data suggest the hypothesis of liver metabolism of plasma DAO.
Subject(s)
Amine Oxidase (Copper-Containing)/blood , Liver/metabolism , Adult , Amine Oxidase (Copper-Containing)/urine , Animals , Bile/enzymology , Female , Heparin/pharmacology , Humans , Kidney/enzymology , Male , Middle Aged , Perfusion , Placenta/enzymology , Rats , Rats, Inbred Strains , SwineABSTRACT
Diamine oxidase activity was determined in twenty-seven samples collected from normal subjects and from patients with renal failure. The enzyme activity was absent or very low in the urine samples of normal subjects. The highest diamine oxidase activity was found in the patients affected with nephrosis, the Fanconi syndrome and renal transplantation, showing a relationship between urinary enzymatic activity and tubular damage, in accordance with the localization in the convoluted tubules.
Subject(s)
Amine Oxidase (Copper-Containing)/urine , Kidney Diseases/enzymology , HumansABSTRACT
Diamine oxidase activity was measured in plasma or urine in 12 normal men, 4 men with chronic liver or heart disease, 13 men with chronic renal failure, and 12 men undergoing maintenance hemodialysis. Also in five studies in 4 patients, plasma diamine oxidase activity and total amine levels were measured at hourly intervals during a hemodialysis treatment. Plasma diamine oxidase activity was normal in patients with liver or heart disease and was at least three times normal in chronically uremic patients and in patients undergoing maintenance hemodialysis. Plasma diamine oxidase activities before and after a hemodialysis therapy were similar and did not change during dialysis until the 4th hour when they fell transiently; plasma total amine levels, which were elevated initially, tended to rise during the 4th hour of dialysis. Urinary diamine oxidase activity was reduced in the chronically uremic patients as compared to normal subjects. These observations are consistent with three alterations in diamine oxidase in patients with renal failure: activity (a) is increased in plasma of chronically uremic patients and those undergoing maintenance hemodialysis, (b) does not increase normally in response to heparin administration during dialysis therapy, and (c) is reduced in urine of chronically uremic patients.
