Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nature of the stationary band of alkaline phosphatase, which occurs on starch gel electrophoresis of sera from patients with biliary obstruction, has been examined. Stationary alkaline phosphatase was eluted from Sepharose 4-B gel close to the void volume and together with the plasma membrane enzymes, nucleotide pyrophosphatase and 5'-nucleotidase, and with lipoprotein-X. Electron microscopy of concentrates of stationary alkaline phosphatase, prepared by ultracentrifugation and gel filtration, showed large (0.3--1 mum diameter) and small structures (30-70 nm diameter) by negative staining. The activity of the stationary alkaline phosphatase was associated in fixed sections with particles of about 10 nm X 40 nm resembling those of lipoprotein-X. It is suggested that the stationary alkaline phosphatase does not move into starch gel during electrophoresis because it is particulate. In agar electrophoresis the alkaline phosphatase which was stationary on starch gel moved towards the cathode with lipoprotein-X.
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PMID:Serum alkaline phosphatase, nucleotide pyrophosphatase, 5'-nucleotide and lipoprotein-X in cholestasis. 17 32

Serial measurements of alkaline phosphatase and 5'-nucleotidase multiple forms in two patients undergoing surgical procedures to release biliary obstruction suggested an inverse relationship between high-M(r) isoforms and serum bile acids concentrations. Furthermore, the study of several groups of patients with cholestatic disorders confirmed this inverse correlation. Mechanisms responsible for these observations are discussed.
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PMID:Changes in alkaline phosphatase and 5'-nucleotidase multiple forms after surgical management of biliary obstruction. 162 1

In 18 horses there was no effect of age or sex on plasma activities of gamma-glutamyl transferase (gamma-GT), 5'-nucleotidase (5'-NT) and leucine aminopeptidase (LAP). All the enzymes were equally stable after storage for one month at -20 degrees C and there was no significant difference between their activities in serum and plasma in clinically normal horses. The pattern of release of gamma-GT, 5'-NT and LAP into plasma was studied in 114 horses which had a variety of orthopaedic, gastrointestinal, cardiovascular and hepatic (necrosis, lipidosis, neoplasia and cirrhosis) conditions. A definitive diagnosis of hepatic disease was established by histological examination of the liver. gamma-GT and 5'-NT were leaked into plasma in hepatic disease and gamma-GT was the more sensitive indicator of liver damage. There was some evidence that gamma-GT and 5'-NT plasma activities may increase in hepatic necrosis as well as in biliary obstruction. LAP was insensitive and not hepatic specific in the horse.
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PMID:Observations on gamma-glutamyl transferase, 5'-nucleotidase and leucine aminopeptidase activities in the plasma of the horse. 256 9

Biliary obstruction in the rat causes known biochemical and morphological abnormalities. These abnormalities might be caused simply by retention of biliary constituents or might require other factors such as high biliary pressure, interruption of the normal flux of fluid, ions, and other biliary constituents through the hepatocyte and/or changes in intracellular concentrations, binding, and distribution of biliary constituents. We studied a choledochocaval (CC) fistula rat model characterized by complete biliary retention without bile stasis. CC fistula animals were compared with biliary obstructed rats over a 46-hr period. Bile flow and bile acid excretion rate reached high levels by hour 5 and remained high in CC fistula rats. Urinary bile acid excretion, shrinkage of the rapidly exchangeable bile acid pool, and serum bile acid and bilirubin concentrations were equivalent in the two models. Serum cholesterol concentration was higher and serum alkaline phosphatase and 5'-nucleotidase activities lower in obstructed rats. The percentage of beta-muricholate rose and the percentage of cholate decreased in bile acid from obstructed rats. This was associated with increased microsomal 6 beta-hydroxylase activity. Bile acid composition and microsomal 6 beta-hydroxylase activity changed little in CC fistula rats. Morphological examination revealed greater damage in obstructed rat livers. These data indicate that factors other than simple retention of biliary constituents contribute to the abnormalities observed in extrahepatic biliary obstruction.
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PMID:Similarities and differences between models of extrahepatic biliary obstruction and complete biliary retention without obstruction in the rat. 684 Jun 84

Human recombinant tumor necrosis factor was administered to rats in small doses to determine whether it causes changes in the activity of liver enzymes similar to those observed in cancer growing extrahepatically. Intraperitoneal injection of increasing doses of tumor necrosis factor (20-100 micrograms/kg/day for 5 days) resulted in a 20-50% decrease in hepatic alanine aminotransferase (P < or = 0.05), a 10-20% decrease in aspartate aminotransferase (P < or = 0.04), and a 50-200% increase in alkaline phosphatase (P < or = 0.02). The activity of hepatic 5'-nucleotidase was unchanged. In the serum, there was no significant change in the activity of any of the enzymes. Histologically, there was no damage detectable by light or electron microscopic examination of the liver, and no evidence of biliary obstruction. However, in frozen liver sections stained histochemically for alkaline phosphatase, there was a dramatic increase in the activity of this enzyme in hepatocytes, which was confined to the bile canaliculi. There was also a 3- to 9-fold increase in the mitotic activity of hepatocytes. Comparable changes have been reported in the tumor-free liver of animals with cancer.
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PMID:Tumor necrosis factor induces enzymatic changes in liver comparable to those in extrahepatic cancer. 850 61

Biliary obstruction, produced by common bile duct ligation or alpha-naphthylisothiocyanate (ANIT) treatment in rats, has been associated with the development of type I biliary epithelial cell (BEC) hyperplasia. However, the exact mechanism(s) by which bile duct obstruction lead(s) to this proliferative lesion are not clear. The present studies were designed to determine if cholestasis, in the absence of biliary obstruction, would result in type I BEC hyperplasia. Male Sprague-Dawley rats were given a single oral dose of 150 mg/kg ANIT or i.v. doses of estradiol glucuronide (E2-17G; 21 mumol/kg/h for 48 h) to produce obstructive and non-obstructive cholestasis, respectively. E2-17G treatment resulted in cholestasis that was comparable in extent and duration to that observed following ANIT treatment. E2-17G and ANIT treatments produced comparable increases in serum bile acids (55- to 60-fold) and activities of ALT (36- to 38-fold), ALP (4- to 5-fold), and 5'-nucleotidase (7- to 11-fold), respectively, compared to controls. Both ANIT and E2-17G also increased serum bilirubin concentrations. ANIT treatment resulted in significant increases in biliary glucose concentrations that were associated with BEC damage/necrosis and obstruction of the bile duct lumen. Conversely, no evidence of BEC damage was observed in E2-17G-treated rats. Nonetheless, BEC hyperplasia was observed in the majority of rats following treatment with either ANIT or E2-17G, assessed by light microscopy and by BrdU immunohistochemistry. These data indicate that E2-17G treatment produces nonobstructive cholestasis and type I BEC hyperplasia, suggesting that biliary obstruction is not a prerequisite for type I BEC hyperplasia in rats. Differences in the time of onset of hyperplasia were observed: hyperplasia was noted immediately following 48 h of E2-17G-induced cholestasis but occurred several days after ANIT-induced cholestasis had subsided. Since the magnitude/duration of cholestasis was similar in the two models but the temporal association between cholestasis and type I BEC hyperplasia were different, these data suggest that the proliferative stimulus may be different in the two models and that E2-17G-induced type I BEC hyperplasia may not be attributed solely to cholestasis.
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PMID:Bile duct obstruction is not a prerequisite for type I biliary epithelial cell hyperplasia. 985 2