Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Physicochemical studies performed on alpha-2-macroglobulin were correlated with the biological activities of this protein. Equilibrium dialysis of the binding of 65Zn by alpha-2-macroglobulin at pH 7.9 showed heterogeneous binding which could be attributed to two classes of binding sites. The site of greatest affinity for zinc had an apparent stoichiometry (n1 in gatoms/mol of alpha-2-macroglobulin monomer) of 12 and an apparent association constant (K1) of 3.06.10(7). The second binding site had an n2 of 60 and K2 of 1.32.10(5). The trypsin binding activity of alpha-2-macroglobulin did not depend on the presence of zinc in this protein since all but traces of this metal could be removed by EDTA without loss of trypsin binding activity. Saturation of site 1 with zinc did not affect the trypsin binding activity of alpha-2-macroglobulin, but binding of the metal by site 2 progressively decreased the trypsin binding activity by causing an irreversable association of the alpha-2-macroglobulin molecules. Removal of excess zinc from alpha-2-macroglobulin did not restore its trypsin binding activity. Our results also indicate that the high zinc content of alpha-2-macroglobulin (320--770 microgram/g protein) reported in the literature is an artifact and that native alpha-2-macroglobulin contains approximately 150--180 microgram Zn/g protein.
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PMID:Binding of zinc to alpha-2-macroglobulin and its role in enzyme binding activity. 7 85

Significant increases of serum alpha-2-macroglobulin (alpha-2-M) were detected in narcotic addicts presenting at a methadone treatment center. The mean alpha-2-M level was 341 +/- 14 mg/dl compared with 231 +/- 8 mg/dl in normal persons (p less than 0.01). In a comparable group of alcoholics with laboratory evidence of hepatic dysfunction the mean alpha-2-M level was 208 +/- 10 mg/dl. Although the serum immunoglobulin M content was also substantially elevated in the narcotic-addict group, no correlation was obtained between the serum content of this protein and alpha-2-M. Similarly, no correlation between alpha-2-M level and serum zinc content was observed. When the values of the trypsin-binding activity of serum measured in 13 addicts, 15 alcoholics with laboratory evidence of hepatic dysfunction, and 16 normal subjects were plotted against the amount of alpha-2-M measured in the same subjects, a linear correlation was obtained between trypsin-binding activity and alpha-2-M. Thus, the significantly increased serum trypsin-binding activity observed in the addicts is that which might be expected if normal alpha-2-M is being accumulated in large amounts as a result of increased macroglobulin synthesis.
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PMID:Hyper-alpha-2-macroglobulinemia in narcotic addicts. 7 76

The present experiments demonstrate that animals carrying large peripheral intramuscular tumours were free of spontaneous pulmonary metastases. Secondaries in the lung emerged, however, after administration of agents such as trypsin, 10% dextrose or antiserum to alpha-2-macroglobulin (AMG). Such metastases also appeared in animals treated with trypsin after amputation of the tumour-bearing limb. It is believed that the pulmonary vessels of tumour-bearing animals are lined with a layer of tumour-associated AMG. The presence of this peptide on vascular endothelium blocks the transmigration of tumour cells. Tumour emboli may remain dormant, i.e. unattached, in the vascular lumen. Agents inactivating AMG or enhancing vascular permeability (proteases, antisera to AMG or vasodilators) may promote the emergence of a latent tumour cell into an overt state. This is confirmed by the above experiments and by the microscopic appearance of the pulmonary vessels of test animals (shift of tumour cells from the intravascular to the perivascular space). It is suggested that latency is determined by the state of permeability of the vessels harbouring tumour emboli.
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PMID:On the latency of tumour cells. 8 78

Alpha-1-antitrypsin deficiency is responsible for emphysema in adults. The genetic polymorphism of this protein (Pi system) is used to detect these deficiencies. The relationship between the serum protease inhibitory capacities and M, MZ and Z Pi phenotypes was investigated. 120 sera including 31 M, 33 MZ and 56 Z were studied. The alpha-1-antitrypsin concentration varied according to the Pi phenotype, the sex and the health of the subject. The alpha-2-macroglobulin level did not depend on the Pi phenotype. The trypsin inhibitory capacity fluctuated with the age and the health of the subject, but did not faithfully represent the Pi phenotype. In contrast, the elastase inhibitory capacity depended only on the Pi phenotype. The relationship between alpha-1-antitrypsin levels and the serum elastase inhibitory capacities was linear. Canonical analysis was employed to determine the relative contributions of each antiprotease to the two inhibitory capacities. It appeared that the elastase inhibitory capacity was influenced more by the alpha-1-antitrypsin level while the trypsin inhibitory capacity was more sensitive to alpha-2-macroglobulin.
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PMID:Tryptic and elastolytic inhibitory capacities of serum from various Pi phenotypes. 8 98

The proteolytic activity of different proteinases during chronic otitis media can be inhibited by alpha-2-macroglobulin and alpha-1-antitrypsin. A new low molecular (13,000) acid stable and polyvalent proteinase inhibitor could be investigated in the middle ear secretion from patients with cholesteatoma and chronic otitis media. We believe that this inhibitor is identical with the low molecular inhibitor of bronchial mucus and the nasal fluid. This inhibitor shows a high anti proteolytic capacity and can inactive trypsin, chymotrypsin, pronase and leucocytic preoteinases. The inhibitor is not detectable in any case. We could find it in 55 cases, three specimens of middle ear secretions obtained no acid stable inhibitor. It is present in the secretion in a masked form by in situ-reaction with leucocytic proteinases. By denaturating deproteinizing it is liberated out of the complex with proteinases and can be measured. The investigations demonstrate that the level of the inhibitor varies during the course of a chronic otitis media. In the postoperative phase the inhibitor concentrations were clearly higher than preoperatively. A steep drop of inhibitor can be observed in cases of chronic otitis with the symptomatology of an acute inflammation. In cases with a chronic inflammation the inhibitor level seems to remain low. The decrease of the inhibitor is explained as a using up effect during reaction between inhibitor and leucocytic proteinases. We believe that this inhibitor in the middle ear secretion results from a limited proteolysis and splitting of inter-alpha-trypsin inhibitor by a proteolytic enzyme, possibly by kallikrein.
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PMID:[The investigation of a low molecular acid stable proteinase inhibitor in the middle ear secretion (author's transl)]. 14 Sep 59

A naturally occurring competitive inhibitor of pig kidney renin has been identified in human plasma. The inhibitor was shown to be alpha-1 anti-trypsin and the effect in vitro on the renin activity was examined. The slope in the Hill plot is compatible with the assumption of one-site competitive inhibition. Other proteinase inhibitors, such as alpha-2-macroglobulin and C1 inactivator, however, have no inhibitory effect on the renin-angiotensinogen reaction.
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PMID:alpha-1-Anti-trypsin, an inhibitor of renin. 108 51

We performed serologic and synovial investigations in rheumatoid (Latex 1/1280, 1/640, negative and Waaler Rose 1/1024, 1/512, negative), non-rheumatoid and control lots. The immunological results were correlated with ultrastructural changes found in the synovial fluid (SF) at the same titres of rheumatoid factor (RF). The pathologic values of the circulating immune complexes (CIC) (mean = 108.05 U), IgM (mean = 420 UI/ml), IgG (mean = 355.36 UI/ml), and anti-collagen II antibodies (mean = 558.6 U) were present at high titres of RF (Latex 1/1280, Waaler Rose 1/1024). These cases had also major ultrastructural changes of the nucleus and cytoplasm. We inferred from this the implication of the immune factors in the etiology and pathology of the Rheumatoid Arthritis (RA). The high, titres of RF were correlated with pathologic values of the C-reactive-protein (CRP) (mean = 13.31 mg%) and alpha-1-acid glycoprotein (A-1-GA) (mean = 158.3 mg%). The decline of the complement fraction C3 from the synovial fluid in RA confirms the immune character of the rheumatoid synovitis and may be useful in the diagnosis process. The significantly lower concentrations of the protease inhibitors alpha-1-anti-trypsin (A-1-AT) (mean = 165.1 mg%) and alpha-2-macroglobulin (A-2-M) (mean = 129.6 mg%) in synovial fluid suggest a diminution of the anti-proteasic activity due to local immune conflict.
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PMID:Some humoral immunological aspects of the rheumatoid arthritis correlated with the ultrastructural changes of the rheumatoid synovial fluid. 128 62

Inflammatory aneurysms of the abdominal aorta (IAA) comprise 10-15% of all aortic aneurysms (AA) but their aetiology and pathogenesis are obscure. Destruction of mural elastin is a prominent feature of IAA, and both increased elastolysis and decreased inhibition of elastolysis have been implicated. In order to study these factors, we have examined the peripheral blood of three groups of patients; 15 with inflammatory aortic aneurysms (IAA), 61 with simple aortic aneurysms (SAA) and 35 with aorto-iliac occlusive disease (OD). In all cases, alpha-1-anti-trypsin (A-1-AT), alpha-2-macroglobulin (A-2-MG), elastase inhibitory activity (E.I.A.), elastase-anti-trypsin complex, C-reactive protein (CRP), caeruloplasmin (CP) and plasma viscosity were measured. Patients with IAA had a significantly higher plasma viscosity (Mann-Whitney, p less than 0.05), E.I.A. (Mann-Whitney, p less than 0.01) and levels of A-1-AT, CRP, CP and elastase/anti-trypsin complex (Mann-Whitney, all p less than 0.05) than patients in the other two groups. There was no difference in the levels of A-2-MG between any of the groups. This study refutes the theory that reduced inhibition of elastase activity predisposes to the formation of SAA. In patients with IAA, raised marker levels indicate ongoing destruction of elastin, and suggest a difference in pathogenesis between IAA and SAA. The study also suggests that IAA are highly active metabolically, as opposed to the more degenerative SAA.
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PMID:Metabolic activity in inflammatory and non-inflammatory aneurysms of the abdominal aorta. 137 41

Hemorrhagic shock caused by gastrointestinal bleeding in seven pigs and by external bleeding in another six pigs and cardiogenic shock induced by intravenous infusion of the tricyclic antidepressant drug nortriptyline in yet another eight pigs caused a significant increase in serum cationic trypsin-like immunoreactivity together with formation of complexes between cationic trypsin, on the one hand, and alpha-2-macroglobulin and alpha-1-antitrypsin, on the other hand, compatible with what happens in acute pancreatitis.
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PMID:Effect of hemorrhagic and nortriptyline-induced shock on the porcine pancreas as evaluated by changes in serum cationic trypsin-like immunoreactivity. 241 78

The technique of immunoelectrophoresis (IEP) was used to examine polymorphism of the endopeptidase inhibitor alpha-2-macroglobulin (alpha 2M) by measuring its electrophoretic mobility. Examination of the variability of the method showed that a large intra- and inter-plate variation occurred (3.3 and 11.6%, respectively). It was also shown that alpha 2M from plasma moves significantly slower than that from serum and that the mobility of alpha 2M from plasma can be increased to that of serum by treatment with trypsin. Upon comparing sera, plasma and synovial fluids from a control group (normal subjects and patients with osteoarthritis) with a group of patients with rheumatoid arthritis, no difference in alpha 2M mobility could be demonstrated. It is concluded that genetic polymorphism of alpha 2M cannot be detected by the technique of IEP.
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PMID:Can genetic polymorphism of alpha-2-macroglobulin be detected by immunoelectrophoresis? A study using sera, plasma and joint fluids from patients with rheumatoid arthritis and controls. 242 67


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