Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antishock effect of N6, O2-dibutyryl cyclic AMP (DBcAMP) Was investigated in rats subjected to Noble-Collip drum trauma and compared with effects of hydrocortisone and Trasylol. Results obtained are as follows. 1)Hydrocortisone and Trasylol administered 1 hr before initiating drumming improved the survival rate from traumatic shock with concomitant reducton of levels of acid phosphatase and beta-glucuronidase in circulating blood. DBcAMP administered i.p. immediately after trauma also improved the survival rate to the same extent as did Traylol or hydrocortisone, while no inhibitory effects were observed on acid phosphatase and beta-glucuronidase. 2)The rectal temperature fell significantly after suffering trauma, and the rats with greater fall in rectal temperature had poorer chance for survival. The fall in rectal temperature was considerably prevented by DBcAMP in a dose of 0.5 mg/100 g body weight (b.w.). 3)DBcAMP induced a rise in plasma insulin level (IRI) and insulin/glucose ratio (I/G) in shock rats, and the elevation in blood lactate/pyruvate ratio (L/P) and excess lactate otherwise observed after trauma were satisfactorily prevented by DBcAMP administration. It is concluded that the antichock effects of DBcAMP primarily resulted from improvements of the intracellular metabolism induced by its easy passage through the cell membrane and its cAMP like action, while any preventive action was not observed against elevation of lysosomal enzymes in the circulating blood.
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PMID:Experimental study of dibutyryl cyclic AMP: its antishock effects observed in traumatic shock rats. 18 67

The pattern of lysosomal enzyme activities in isolated pancreatic islets was studied in 3 different strains of mice, NMRI, CBA, and C-57, and related to the in vivo insulin release following injection of the insulin scretagogues glucose and carbachol. It was observed that the relative specific activities among the islet enzymes studied did not show the same pattern in the different strains although beta-gluc-ronidase always displayed the lowest activity. Comparison between the strains revealed that acid phosphatase activity was of the same magnitude in all 3 strains. Islet activities of acid amyloglucosidase, beta-glucuronidase, and N-acetylglucosaminidase, however, were largest in NMRI, intermediate in CBA, and lowest in C-57. This activity pattern roughly correlated with the insulin secretory response to an intravenous injection of glucose, whereas insulin release induced by the cholinergic agonist carbachol was of similar magnitude in all strains.
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PMID:Pattern of islet lysosomal enzyme activities and insulin secretory response. 33 99

Non-latent (free) activities of two lysosomal enzymes (acid phosphatase and beta-glucuronidase) and urea production were measured in purified rat liver parenchymal cells incubated in the presence and absence of insulin. Non-latent enzyme activity was measured by including 0.25M sucrose in the assay mixtures to provide osmotic protection to the lysosomes. Total enzyme activity was estimated with Triton X-100 in the homogenates. Insulin was found to inhibit ureogenesis and to reduce non-latent lysosomal enzyme activity in the hepatocytes in vitro. Our data support the idea that insulin inhibits autophagy in rat liver parenchymal cells. Such an effect of insulin may also explain the inhibitory action of insulin on urea production in the rat liver.
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PMID:Influence of insulin on lysosomal activity and urea production in isolated parenchymal cells from rat liver. 103 39

Rats were injected with labeled Kunitz protease inhibitor and killed at various times thereafter. Radioactivity was measured in various fractions of kidney homogenates in order to study the time-dependent fixation to different cell organelles, expecially the transition from the brush border to lysosome fraction. With short survival periods (up to 5 min), the renal protease inhibitor is recovered nearly completely with the brush border fraction. With longer periods, a shift towards particles with higher densities and higher beta-glucuronidase activities takes place. Similar results have been achieved with insulin. Lysosomes were prepared and subfractionated following i. v. administration of the protease inhibitor or insulin. The radioactivity of the peptides was found in the lysosomal range of density. According to our present and previous results, the renal pathway of the protease inhibitor consists of 3 steps: binding to the brush border, reabsorption into micropinocytotic vesicles and phagosomes, and final enrichment in phagolysosomes with subsequent degradation. We suggest this type of transport to be representative for peptides in general.
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PMID:In vivo interaction of the Kunitz protease inhibitor and of insulin with subcellular structures from rat renal cortex. 107 84

Kinetic studies of the histochemical and histoenzymatic behavior of rabbit pancreatic parenchymas were performed 5, 30 and 90 days after Wirsung duct ligation. In control pancreas, some enzyme activities (EA) were more prominent in Langerhans islets [glucose-6-phosphatase, glucose-6-phosphate dehydrogenase (DH), isocitrate DH, glycerol-3-phosphate DH, NADPH DH], others were strongly marked in acini and ducts (alkaline phosphatase, beta-glucuronidase, acid esterase aryl-sulfatase). Histochemical and enzyme abnormalities observed in experimental rabbits reflect the post-ligation degenerative and reactive processes in both exocrine and endocrine pancreas: (1) the decrease in Krebs cycle and pentose pathway linked EA and the increased lysosomal and acid phosphatase EA reflect early (day 5) degeneration and necrosis of islets and acini (day 30); (2) proliferative processes in developed ductal epithelia are shown by an increase in both glycolytic and lysosomal EA (days 30 and 90); (3) connective tissue neogenesis and interstitial fibrosis occurred as shown by activated beta-glucuronidase, aryl-sulfatase, alkaline phosphatase and increased ribonucleoproteins and glycoaminoglycans contents (day 30); (4) on day 90, the neoformed cell clusters presenting glucose-6-phosphatase positivity (B-cell marker) are seen in the pancreas remnant. At the same time, blood insulin level increases correlated with a decrease of hyperglycemia.
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PMID:Cell features in pancreas of prediabetic and diabetic rabbits after Wirsung duct ligation. Histochemical and histoenzymatic studies. 233 24

Polymorphonuclear neutrophils' chemotaxis, surface charge, superoxide anions generation, NBT (nitro blue tetrazolium) reduction and intracellular lysozyme, and beta-glucuronidase content were estimated in patients with type I diabetes mellitus in a similar state of metabolic control. The chemotaxis of diabetic cells toward bacterial chemotactic factors was similar to controls, whereas migration toward complement-derived chemoattractants was significantly reduced. Polymorphonuclear neutrophils isolated from diabetic patients, when unstimulated, produced significantly greater amounts of superoxide anions and reduced NBT more efficiently. They also revealed reduced surface charge and lower intracellular content of lysozyme, whereas beta-glucuronidase content was similar to controls. The results obtained seem to indicate that neutrophils in patients with insulin-dependent diabetes manifest signs of being in the activated state. The possible mechanisms of such stimulation are discussed.
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PMID:Evidence of polymorphonuclear neutrophils (PMN) activation in patients with insulin-dependent diabetes mellitus. 282 47

Whereas the phosphorolytic breakdown of liver glycogen is known to be of great physiological importance, the functional role of the hydrolytic glycogenolysis in the lysosomal system is less well understood. In the present study the effects of fasting, alpha- and beta-adrenoceptor antagonism and insulin-induced hypoglycaemia on liver lysosomal glycogen-hydrolysing enzyme activity were investigated in mice. In freely fed mice the glycogen-hydrolysing activity (acid amyloglucosidase) was only 50% of the maltose-hydrolysing activity (acid maltase). Starvation for 24 h reduced the acid amyloglucosidase activity by approximately 30% (P less than 0.001), whereas the activities of acid maltase, acid phosphatase and beta-glucuronidase appeared unaffected. N-acetyl-beta-D-glucosaminidase activity was moderately (20%; P less than 0.01) enhanced by fasting. Thus, liver lysosomal enzyme activities may change independently of each other during fasting. Further, during short-term hypoglycaemic conditions (45 min) induced by endogenous or exogenous insulin, the activity of liver acid amyloglucosidase was found to be moderately reduced (15-20%). Blockade of alpha- and beta-adrenoceptors by phentolamine and propranolol did not result in any apparent influence on acid amyloglucosidase activity except for the indirect effect exerted by the phentolamine-induced hypoglycaemia. A moderate negative correlation (r = -0.51; P less than 0.001) between total liver glycogen concentration and acid amyloglucosidase activity was observed in a series of 43 freely fed NMRI mice. Our data show that in mouse liver the acid maltase activity predominates over the acid amyloglucosidase activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glycogen and glycogen-hydrolysing lysosomal enzyme activity in mouse liver: effects of fasting, adrenoceptor antagonism and insulin-induced hypoglycaemia. 289 Feb 62

It is suggested that the important drugs rifampicin and halothane and the raised glucose levels in diabetes mellitus exert injurous effects on cells through a lysosomal mechanism. Further evidence is given of by time rifampicin induction of beta-glucuronidase and beta-N acetylglucosaminidase and its possible relation to hepatitis and pancreatitis. On the basis of preliminary data halothane may cause hepatitis connected to lysosomal enzyme release in the presence of other aggravating factors common to the perioperative period. The onset of diabetic vascular complications may be related to the similar raised levels of lysosomal enzymes found in insulin, drug and diet controlled disease. Release of these enzymes into plasma may be a marker of important changes in the lysosome, whether due to enzyme induction or damage, and could be a primary mechanism of many disease processes including some thought to be mainly autoimmune in character. Routine estimation in the clinical laboratory along with existing cytoplasmic and microsomally derived enzymes in the chemical screen would be a useful way of surveying lysosomal changes in the wide spectrum of disease in a general hospital.
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PMID:Rifampicin, halothane and glucose as mediators of lysosomal enzyme release and tissue damage. 341 3

Lysosomal enzyme activities in pancreatic islets of obese hyperglycemic ob/ob mice aged 3 to 6 months were investigated and compared with those of normal lean NMRI mice of the same age. It was observed that the glycogenolytic glucose-producing hydrolase acid amyloglucosidase displayed a fivefold higher activity in the islets of obese mice than in the islets of normal NMRI mice. However, other islet lysosomal enzyme activities measured, such as N-acetyl-beta-D-glucosaminidase and beta-glucuronidase, were of the same magnitude in both obese and lean mice. A starvation period of 24 hours induced a significant depression of islet acid amyloglucosidase activity in obese as well as lean mice, whereas the activities of N-acetyl-beta-D-glucosaminidase and beta-glucuronidase were unaffected. Further, the activities of other types of islet lysosomal enzymes, such as acid phosphatase and cathepsin D, were also measured in obese mice. These activities were not found to be affected by the actual fasting period. A good correlation (r = 0.815; P less than 0.01) was observed between islet acid amyloglucosidase activity and plasma insulin concentrations in obese mice, whereas no such relationship was apparent with regard to other islet lysosomal enzyme activities recorded. Acid amyloglucosidase activity in liver tissue of the obese mouse was about 30 times lower than that of islet tissue. Further, the activity of liver amyloglucosidase was of the same order of magnitude in obese and lean mice. Similarly, other lysosomal enzyme activities in the liver of obese and lean mice were not strikingly different.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lysosomal enzyme activities in pancreatic islets from normal and obese hyperglycemic mice. 391 27

Diabetes induced by alloxan at day 6 of gestation in Wistar rats produced decreased fetal growth, delayed skeletal ossification, decreased fetal kidney beta-glucuronidase, and an increased frequency of fetal birth defects which correlated with the degree of diabetic control. Offspring of severely diabetic mothers (mean blood glucose greater than 501 mg/dl) sacrificed at 20 days had a mean weight of 2.12 +/- 0.16 g, a mean of 1.8 +/- 0.46 caudal ossification centers, and a 28% incidence of birth defects as compared to 3.70 +/- 0.22 g, 5.9 +/- 0.42 caudal centers, and 1.1% defects for controls. Offspring of severely diabetic mothers sacrificed at 21 days had mean numbers of caudal and sternal ossification centers which did not significantly differ from controls, indicating that decreased ossification observed at 20 days of gestation is a delayed developmental sequence which is mostly corrected by 21 days. Offspring of moderately diabetic (mean blood glucose 300-500 mg/dl) and insulin-treated dams (mean blood glucose 152-168 mg/dl) had intermediate degrees of growth or ossification delay and birth defect frequency at both the 20- and 21-day sacrifices. Maternal diabetes also retards the developmental increase in fetal kidney beta-glucuronidase such than 20-day offspring of severely diabetic mothers had a mean specific activity of 1.1 nmol/min/mg compared to 3.0 nmol/min/mg for controls. The results support prior studies in rodents suggesting a progression of early growth delay, altered developmental sequences, and birth defects in diabetic pregnancy. This progression is suggested as a common teratogenic mechanism which has implications for evaluating analogous pregnancies in man.
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PMID:Delayed developmental sequences in rodent diabetic embryopathy. 408 Apr 55


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