Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.5.1.4 (deaminase)
 5,113 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Asymptomatic identical twins were found to show the prolonged activated partial thromboplastin time, which was corrected by addition of normal, Hageman factor deficient or Fletcher trait plasma but not corrected by Fitzgerald or Williams plasma. The prolonged activated partial thromboplastin time was also corrected by addition of highly purified bovine high molecular weight kininogen but not by low molecular weight kininogen. When total kininogen was measured as the amount of bradykinin released by trypsin on acid treated plasma, only trace amount was detected in Fujiwara and Williams plasmas, although Fitzgerald plasma showed approximately 50% of the total kininogen of normal plasma level. Acetone-kaolin activated amidase activity of plasma kallikrein was not generated by Fujiwara plasma. Substitution with normal plasma in various ratios showed plasma kallikrein activity proportionally to the normal plasma contents. Extrapolation with the values at 120 min after activation gave the prekallikrein content of Fujiwara plasma as 30% of the normal value.
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PMID:Fujiwara trait: the first case of kininogen deficiency in Japan. 51 63

Blood pressure (BP), plasma prekallikrein (PK), and the extent of activation of factor XII (XII-ACT) were studied after the intravenous injection into rats of dextran (Macrodex), the ionic radiographic contrast substance iodipamide (Biligrafin), or the non-ionic contrast substance iohexol (Omnipaque). After acetone activation plasma kallikrein was assayed as plasminogen activator, BAEe esterase or S-2302 amidase, and factor XIIa was assayed as kaolin-activated prekallikrein activator. Dextran induced a strong and lasting hypotension, preceded by significant lowerings in PK and XII-ACT. Iodipamide induced a rapid and dose dependent BP fall, no change in plasma PK, but a slightly reduced XII-ACT. Iohexol induced no significant alterations, neither in BP, nor in plasma parameters. Pretreatments of the rats with iodipamide abolished the dextran-induced reductions in PK and XII-ACT, and almost blocked the fall in BP. We conclude that the ionic contrast substance iodipamide is capable of blocking dextran shock in the rat by preventing an activation of the contact activating system in plasma.
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PMID:Effects of intravenous radiographic contrast media on the blood pressure and on factors of the contact activation system in the rat. 243 54

Acetylcysteine (AC) injected intravenously into rats (200 mg/kg) had no effect on blood pressure, but significantly inhibited dextran-induced (40 mg/kg) blood pressure fall. Injection of AC also reversibly blocked the activation of prekallikrein (PK) normally obtained in plasma incubated with acetone. Kallikrein was assayed as plasminogen activator, S-2302 amidase and BAEe esterase. Also the activation of factor XII to factor XIIa, assayed as prekallikrein activator, was strongly inhibited in AC-treated rats. It is suggested that the partial blockade of dextran-induced shock is correlated with an inhibition of activation of PK and factor XII. Previous experiments had demonstrated an extensive, but reversible in vitro inhibition of human plasma kallikrein by AC. In view of such data it is concluded that the present results obtained with AC in rats are probably due to an inhibition of plasma kallikrein and its activation of factor XII.
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PMID:Acetylcysteine in rats: inhibition of activation of prekallikrein and factor XII--protection against dextran-induced blood pressure fall. 243 51

Factor XII was assayed in acetone-treated and kaolin-activated human citrated plasma (total plasma dilution 1.0 + 0.3 v/v during activation with kaolin, 1.8 mg/ml incubate). Measurements were performed with the tetrapeptide Bz-Ile-Glu-Gly-Arg-pNa (S-2222) and with prekallikrein as substrates. The correlation of both methods to another S-2222 based method recently described was good, r = 0.90 and 0.85 for the two methods respectively. Under the assay conditions used, FXIIa was present as a S-2222 amidase that could be blocked by corn inhibitor, whereas plasma kallikrein was found to be present partly as an amidase blocked by a low concentration of soybean trypsin inhibitor, and partly in a functional state not inhibited and adding to the measured level of FXII. The presence of benzamidine 0.7 to 2.1 mM during acetone treatment increased the measured level of FXII assayed both as prekallikrein activator and as S-2222 amidase.
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PMID:Assay of factor XII in human plasma using prekallikrein or the chromogenic peptide S-2222 as substrates--significance of the functional state of plasma kallikrein. 278 41

The fibrinolytic system was studied in normal human plasma containing increasing concentrations of acetone up to 23.4 mmol l-1. Fibrinolytic activity measured as euglobulin clot lysis time [ECLT] and amidase activities toward chromogenic peptide substrates H-D-Valyl-L-Leucyl-L-Lysine-p-nitroanilide 2 HCl [S-2251], designed for plasmin determination, H-D-Valyl-L-Phenylalanyl-L-Lysine-p-nitroanilide 2 HCl [S-2390], designed for the determination of t-PA in plasma via plasminogen activation and H-D-Prolyl-L-Phenyl-Alanyl-L-Arginine-p-nitro-anilide 2 HCl [S-2302], designed for the determination of kallikrein and activated Hageman factor, increased when 15.7 mmol l-1 concentration of acetone was reached. A parallel increase of esterolytic [substrate: naphthol-AS-acetate] activity was observed in euglobulin fractions. Crossed immunoelectrophoresis [CIE] revealed changes in fibrinogen profiles of plasma enriched with acetone as compared to native plasma. These findings suggest that acetone present in plasma in concentrations comparable to those found in some pathological states might activate fibrinolytic system.
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PMID:Enhancement of fibrinolytic activity of human plasma in the presence of acetone. 799 40

The plasma level of factor XII (FXII) was measured in samples from healthy young men. The activated contact factor was assayed as prekallikrein activator (PKA), as S-2222 amidase, and in radial immunodiffusion tests. By removing the bulk of IgG on protein G columns before the activation procedure, the functional activities increased to about 135%. In such test preparations, PAGE immunoblot experiments with polyclonal antibodies against FXII showed, in addition to FXIIa (80 kD), a double band with a molecular weight of about 46 kD. This protein could also be detected with a light-chain-specific monoclonal antibody to FXII, but not with such an antibody directed against its heavy chain. The 46-kD band was also observed in plasma deficient in FXII. The amidase assays indicated that the minor part of FXIIa was present in some kind of association with another protease. To obtain a correct estimation of total FXIIa in the amidase assays a sufficiently high level of FXI was required compared to that of FXII. The PKA assays were generally carried out with a prekallikrein (PK) substrate containing IgG. By replacing this substrate by PK free from IgG additional PKA activity was observed, the activity appearing also in plasma deficient in FXII.
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PMID:Significance of IgG for the activity of factor XII measured in human plasma. 903 54

Protein G columns were used to remove IgG from human plasma, and the effect on levels of factor XII, factor XI and prekallikrein was studied in functional tests. IgG was detected in PAGE immunoblot experiments with Fc-specific antibodies. Removal of the bulk of IgG in a procedure based on a low plasma dilution (1+2.5) allowed the passage of an IgG fraction along with the contact factors. This fraction was found to be present in higher amounts in plasma from patients with Crohn's disease (n=5) than in control plasma (n=12). In a previous study, PAGE immunoblot experiments showed that part of the prekallikrein was removed along with IgG when a higher plasma dilution (1+10.8) was used (Scand J Clin Lab Invest 1999; 59: 55-64). This observation was supported by results in the present work based on parallel assays with the peptide substrates S-2302 and Bz-Pro-Phe-Arg-pNA. The prekallikrein fraction removed was present in a functional state differing from the main part of prekallikrein by yielding kallikrein with a significantly increased activity against the substrate S-2366. This prekallikrein fraction was present in higher amounts in patient plasma than in control plasma. Part of the corresponding amidase activity was blocked by lima bean trypsin inhibitor, suggesting its presence in association with factor XI. The results also indicated that prekallikrein activator activity was connected with this fraction. With the high dilution procedure an extensive removal of IgG from the patient plasma was obtained compared to the control plasma.
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PMID:Removal of IgG from normal plasma and plasma from untreated patients with active Crohn's disease--effect on levels of contact factors. 1088 96