Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.2.1.31 (
beta-glucuronidase
)
7,680
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The biologic role of calcium and guanosine 3':5'-monophosphate (cyclic GMP) in the immunologic secretion of lysosomal enzymes from human neutrophils was studied. Contact of neutrophils with zymosan-treated serum or the divalent cation ionophore A-23187, in the presence of extracellular calcium, resulted in
beta-glucuronidase
(beta-D-glucuronide glucuronosohydrolase,
EC 3.2.1.31
) secretion and a concomitant accumulation of cyclic GMP without any loss of cell viability.
Acetylcholine
(0.1 muM), in the presence of calcium, enhanced the immunologic stimulation of cyclic GMP accumulation and lysosomal enzyme discharge. A marked and rapid association of 45CaCl2 with neutrophils occurred during cell surface contact with zymosan-treated serum, and this effect on calcium association was enhanced with 0.1 muM acetylcholine. The precise mechanism of the neutrophil-calcium interaction is presently not well understood. However, the finding that 0.5-1.0 muM A-23187 also provoked a rapid association of extracellular calcium with neutrophils suggests that calcium mobilization into the intracellular environment may account, at least in part, for this association between cells and calcium. The close temporal relationship between
beta-glucuronidase
secretion, cyclic GMP accumulation, and calcium mobilization during cell contact with membrane active agents such as immune reactants, acetylcholine, and ionophores suggests that these three cellular events bear a cause and effect relationship. On the basis of our findings to date, we propose that the immunologic secretion of lysosomal contents from human neutrophils is signaled by intracellular cyclic GMP and that extracellular calcium, by gaining access to the intracellular processes responsible for cyclic GMP accumulation, serves as the link to stimulus-secretion coupling.
...
PMID:Bioregulation of lysosomal enzyme secretion from human neutrophils: roles of guanosine 3':5'-monophosphate and calcium in stimulus-secretion coupling. 16 9
The influence of autonomic neurohormones on the immunologic release of
beta-glucuronidase
(
EC 3.2.1.31
) from, and the cyclic nucleotide levels in, human neutrophils was determined. Interaction of neutrophils with rheumatoid arthritic, serum-treated zymosan particles in a neutral balanced salt solution at 37 degrees resulted in the extracellular discharge of
beta-glucuronidase
without any loss of cell viability, as indicated by the failure of incubated cells to take up eosin Y or to release cytoplasmic lactate dehydrogenase (EC 1.1.1.27). Epinephrine reduced the release of
beta-glucuronidase
from neutrophils in the presence of zymosan during 2-30 min of incubation and elicited a concomitant elevation of adenosine 3':5'-monophosphate levels. Propranolol, a beta-adrenergic receptor antagonist, but not phentolamine, an alpha-adrenergic receptor antagonist, blocked both actions of epinephrine.
Acetylcholine
stimulated the release of
beta-glucuronidase
, but not lactate dehydrogenase, and provoked a concomitant elevation of guanosine 3':5'-monophosphate levels. Atropine, a muscarinic receptor antagonist, but not hexamethonium, a ganglionic blocker, inhibited both actions of acetylcholine. Interaction of neutrophils and zymosan particles resulted in an elevation of guanosine 3':5'-monophosphate levels within 2 min. These data suggest that intracellular guanosine 3':5'-monophosphate may be involved in mediating the immunologic release of lysosomal enzymes from human neutrophils whereas adenosine 3':5'-monophosphate may inhibit enzyme release. Moreover, autonomic neurohormones appear to be capable of modulating lysosomal enzyme release by virtue of their capacity to elevate neutrophil cyclic nucleotide levels.
...
PMID:Hormonal control of lysosomal enzyme release from human neutrophils: elevation of cyclic nucleotide levels by autonomic neurohormones. 415 56
We measured the levels of lysosomal enzymes and acetylcholine in Wuchereria bancrofti-infected asymptomatic microfilaraemic human serum, and found a significant decrease in the activity of
beta-glucuronidase
and acid phosphatase compared to normal serum.
Acetylcholine
levels were also decreased during infection. However, after giving diethylcarbamazine (6 mg/kg body wt/day) the level of lysosomal enzymes and acetylcholine increased and reached a normal value after two weeks of therapy. It is proposed that parasites secrete acetylcholinesterase in the circulation which degrades acetylcholine. Since acetylcholine stimulates the release of lysosomal enzymes and phagocytosis, the immune response of the host is suppressed during infection. During diethylcarbamazine (DEC) therapy the parasitic enzyme is inhibited by the drug and the normal level of acetylcholine is resumed, which again stimulates the release of lysosomal enzyme and the process of phagocytosis.
...
PMID:Diethylcarbamazine: effect on lysosomal enzymes and acetylcholine in Wuchereria bancrofti infection. 927 Jul 36
