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

1. Adenosine diphosphate (ADP) and adrenaline caused the aggregation of human platelets suspended in plasma containing citrate anticoagulant and stirred at 37 degrees C. The aggregation occurred in two phases and the second phase was associated with the appearance in the plasma of up to 30% of the ATP and 55% of the ADP present in the platelets. The concentration of ADP appearing in the plasma was up to 7 times the concentration added.2. Radioactivity was released by ADP and by adrenaline from platelets labelled with radioactive 5-hydroxytryptamine; this release was closely correlated with the second phase of aggregation and with the release of nucleotides.3. Acid phosphatase, beta-glucuronidase and adenylate kinase were released to a small extent during second phase aggregation by ADP or adrenaline; thrombin and collagen particles caused significantly greater release of beta-glucuronidase than of either acid phosphatase or of adenylate kinase.4. Morphological changes indicating degranulation of the platelets were observed during the second phase of aggregation produced by adrenaline and by ADP.5. The second phase of aggregation, degranulation of platelets, and the release of nucleotides, of labelled 5-hydroxytryptamine and of enzymes, were all inhibited by concentrations of amitriptyline which did not inhibit aggregation.
 ...
PMID:The release of nucleotides, 5-hydroxytryptamine and enzymes from human blood platelets during aggregation. 564 42

We studied the effects of running-training, heavy exercise and termination of training on the heart weight, the ratio heart to body weight and the cardiac muscle activities of actomyosin ATPase, citrate synthase, succinate dehydrogenase, cytochrome c oxidase, malate dehydrogenase, adenylate kinase and beta-glucuronidase with adult male NMRI-mice. Stable hypertrophy (6-7%), estimated by the ratio heart or ventricle weight to body weight, was achieved by 28 exercises and it was dependent on the running speed (20 vs. 25 m X min-1). The withdrawal of training for 5-61 days did not permanently decrease the heart weight or the heart to body weight ratio to the level of sedentary controls. The activity of enzymes of energy metabolism or actomyosin ATPase were not affected by training, heavy exercise or terminated training. beta-glucuronidase activity slightly (20-25%) increased in the trained animals and remained at a higher level during the period of terminated training. The results suggest that the capacity for aerobic metabolism of normal mice heart is sufficient to meet the enhanced demand for ATP imposed by running-training and that the heart enlargement occurs in equal proportions with the enzymatic potential of the cardiac tissue.
 ...
PMID:Selected enzyme activities in mouse cardiac muscle during training and terminated training. 623 64

Interpretation of biochemical measurements in the human brain after death is complicated by a variety of premortem, perimortem, and postmortem factors. The activity of glutamic acid decarboxylase (GAD) in particular has been found to vary considerably among human brains. In contrast to neurotransmitter-associated enzymes, metabolic enzymes are present in all brain cells and should not be specifically lost by patterned neuronal cell loss such as that which occurs in Parkinson disease. We compared the activity of GAD to that of the metabolic enzymes creatine kinase (CK), adenylate kinase, hexokinase, beta-glucuronidase, and malate, lactate, glucose-6-phosphate, and isocitrate dehydrogenases in 24 regions of six human brains. Of the metabolic enzymes, only CK showed a 5-fold variation approaching that of GAD. Like GAD, CK activity was stable postmortem, but its activity was apparently inversely related to the severity and duration of the preterminal illness. CK may be a useful marker of agonal deterioration.
 ...
PMID:Regional activities of metabolic enzymes and glutamate decarboxylase in human brain. 731 90