Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D03244 (Kaolin)
 239 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Activation of plasminogen-free rat citrated plasma (RCPL-P) with acetone/kaolin yielded BAEe-esterase activities of 0.6--0.8 U/ml. Gel filtration demonstrated one single peak of BAEe-esterase activity (mol. wt. approximately 135000) with a kininogenase-esterase ratio (3.3) close to that known for human plasma kallikrein (2.7). Similarly activated rat citrated plasma (RCPL) revealed on gel filtration an additional esterase peak (mol. wt, approximately 47,000) with a low kininogenase-esterase ratio (0.3), and should accordingly not be used for a BAEe-esterase assay of rat plasma kallikrein. Acetone activation of RCPL-P and of RCPL yielded prekallikrein activator (PKA) activities which were about doubled by treatment with kaolin to 1.9--2.1 and 3.5--4.2 PKA-U/ml respectively. Gel filtration of acetone-activated RCPL-P or RCPL revealed two peaks of PKA activity, mol. wt. approximately 110,000 corresponding to activated factor XII (XIIa), and mol. wt. approximately 33,000 corresponding to XII fragments (XIIf). Kaolin-treatment of acetone-activated RCPL-P, but not of RCPL, caused an extensive fragmentation of XIIa to the 4--6 times more active XIIf. The lower yield of PKA-activity in acetone/kaolin-activated RCPL-P, as compared with activated RCPL, seems to be due to the absence of a factor of significance for the activation of factor XII, which is not plasmin, plasma kallikrein, or high molecular weight kininogen.
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PMID:Prekallikrein activator and kallikrein in acetone- and kaolin-activated rat plasma. 50 39

A mechanism of writhing reaction induced by kaolin, a known activator of factor XII, was studied. Kaolin induced a distinct writhing response, when injected intraperitoneally into mice (2.5 mg/mouse). The response disappeared in 15 min, but it was reproduced by intraperitoneal injection of captopril, 20 micrograms, into mice who had received the injection of kaolin 60 min before. This later response as well as the early one was not produced when mice were pretreated with bromelain (10 mg/kg, intravenously), 30 min before the kaolin administration. Therefore we determined if bromelain, a known depleter of plasma prekallikrein and a high molecular weight (HMW) kininogen, depletes those in mice. Plasma was collected from mice with or without pretreatment of bromelain, and kinin release of these plasma samples was examined by action of kaolin. The bromelain-treated mouse plasma released kinin amount of less than detection limit when activated with kaolin, whereas normal plasma released about 300 ng/ml of kinin of bradykinin equivalent as assessed by rat uterus contraction. Furthermore, activation of prekallikrein by kaolin was observed in mouse plasma as amidase activity to produce fluorescence from the synthetic substrate. It was completely diminished in the presence of soybean trypsin inhibitor. These results suggest that bromelain could deplete the HMW-kininogen in mouse plasma in the same way as in rat plasma. Furthermore, it is assumed that the kinin released from HMW-kininogen by kaolin could be responsible for inducing the writhing response.
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PMID:Kaolin-induced writhing response in mice: activation of the plasma kallikrein-kinin system by kaolin. 261 39

The writhing reaction in mice induced by kaolin, a factor XII activator, was studied. An intraperitoneal injection of kaolin clearly induced a writhing reaction in a dose-dependent fashion, and the reaction disappeared about 10-15 min later. The writhing reaction reached a peak at 5-10 min after the injection of kaolin (0.5 ml/mouse, i.p.; 5 mg/ml saline). A simultaneous intraperitoneal injection of soybean trypsin inhibitor (SBTI, 2.5 mg/mouse) almost completely suppressed the writhing reaction caused by kaolin (2.5 mg/mouse) for the first 10 min. The kaolin-induced writhing reaction was markedly potentiated by a simultaneous intraperitoneal injection of captopril (50 micrograms/mouse). At 60 min after kaolin injection during the disappearance of the writhing reaction, the reaction reappeared when captopril was injected, but reactions observed at this later stage were completely blocked by SBTI. Indomethacin, ibuprofen and alminoprofen inhibited the writhing reaction dose-dependently. Kaolin thus induces a clear and reproducible writing reaction, which might be mainly dependent on the action of bradykinin via activation of factor XII, and should prove to be a simple and convenient model of bradykinin-induced pain for the assessment of analgesic actions.
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PMID:A new writhing model of factor XII activator-induced pain for assessment of non-steroidal anti-inflammatory agents. I. Kaolin-induced writhing in mice. 266 95

Human factor XII, upon exposure to negatively charged surfaces such as kaolin, sulfatides, and heparin, is converted to enzymatic forms, factor XIIa and factor XIIf. Cl inhibitor has been quantitatively demonstrated to be the primary plasma inhibitor of both factor XIIa and factor XIIf. Studies were performed to determine whether the presence of artificial, negatively charged surfaces influenced the ability of Cl inhibitor to inhibit factors XIIa and XIIf. Kaolin and sulfatides slowed the rate of inhibition of factor XIIa by Cl inhibitor 4.8- and 2-fold, respectively, whereas they had no effect on the inhibition of factor XIIf by Cl inhibitor. Heparin in a concentration of 65 U/ml decreased the inhibition rate of factor XIIa by Cl inhibitor, but, at the same concentration, had less of an effect on the ability of Cl inhibitor to inhibit factor XIIf. These studies indicate that negatively charged surfaces protect factor XIIa but not factor XIIf from inhibition from Cl inhibitor. Since the difference between factors XIIa and XIIf consists of the presence of a surface binding region in factor XIIa, the basis of this protection must reside in the surface binding residues of factor XII. These in vitro events suggest that surface-bound factor XIIa may hydrolyze its physiologic substrates, factor XI and prekallikrein, in an environment partially protected from inhibition by Cl inhibitor.
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PMID:Effect of negatively charged activating compounds on inactivation of factor XIIa by Cl inhibitor. 349 11

The kaolin-mediated reciprocal activation of bovine factor XII and prekallikrein was divided into the following two reactions: the activation of factor XII by plasma kallikrein (reaction 1) and the activation of prekallikrein by factor XIIa (reaction 2). The effects of high-Mr kininogen and kaolin surface on the kinetics of these activation reactions were studied. High-Mr kininogen markedly enhanced the rate of reactions 1 and 2 in the presence of kaolin, and the enhancements were highly dependent on the concentrations of the protein cofactor and amount of kaolin surface. For the activation of factor XII by plasma kallikrein (reaction 1), high-Mr kininogen was required when a low concentration of factor XII and kaolin was used. The molar ratio of the protein cofactor to factor XII for optimal activation was found to be approximately 1:1. The apparent Km value and the kcat/Km value for plasma kallikrein on factor XII were calculated to be 4 nM and 5.2 X 10(7) s-1 X M-1, respectively. The activation of prekallikrein by factor XIIa, (reaction 2) proceeded even in the absence of high-Mr kininogen and kaolin. The addition of the protein cofactor and surface to the reaction mixture remarkably accelerated the reaction, and the apparent Km value for factor XIIa on prekallikrein was reduced from 1 microM to 40 nM. Moreover, the kcat/Km value was altered from 7.3 X 10(4) to 1.1 X 10(6) s-1 X M-1). These results suggest that high-Mr kininogen accelerates the surface-mediated activation of factor XII and prekallikrein by enhancing the susceptibility of factor XII to plasma kallikrein, on the one hand, and the affinity of factor XIIa for prekallikrein, on the other hand. Kaolin may play an important role in the concentration and organization of these components on the negatively charged surface.
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PMID:Kinetic studies on surface-mediated activation of bovine factor XII and prekallikrein. Effects of kaolin and high-Mr kininogen on the activation reactions. 387 94

Blood biocompatibility of medical devices is in many ways dependent on surface characteristics and biochemical blood material interactions. In this study, the contact system, in which the activation of factor XII and plasma kallikrein is included, is highlighted. This article describes a simple chromogenic assay to determine the Hageman Factor fragment (HFf, or factor XIIf) and kallikrein activity in vitro. The assay is based on conversion of Z-Lys-Phe-Arg-pNA.2HCl to which human factor XIIf and kallikrein appeared to have a high affinity. To discriminate between the serine proteases factor XIIf and kallikrein to cleave this substrate, aprotinin was added to one of two complementary samples. In this in vitro study, standardized disks from glass, high-density polyethylene (HDPE), polytetrafluoro ethylene (PTFE), and polydimethyl siloxane (PDMS) were studied for their capacity to generate factor XIIf and kallikrein in plasma. Kaolin was used as positive control. On glass disks the highest and on HDPE the lowest generation of factor XIIf and kallikrein were found, both with a ratio of 1:1. On PDMS and on PTFE disks protease activities were intermediate, but with a factor XIIf and kallikrein activity ratio of 1:2 and 1:4, respectively. Apparently because of the hydrophobic surface character of PDMS and PTFE, these surfaces absorb or fail to produce the factor XIIf. This assay appeared to be discriminative even for materials that are considered mild activators of the contact system and can therefore be used as a standard method to qualify biomaterials.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Factor XII fragment and kallikrein generation in plasma during incubation with biomaterials. 752 36