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

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Query: EC:3.4.21.5 (thrombin)
33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Determination of the complement titer in the serum and plasm of 120 patients with chronic liver diseases showed that in eight (7%) patients with cirrhosis of the liver, chronic active or chronic inactive hepatitis complement in the serum was less than half in the plasma. The dissociation of complement serum and plasma was due to cold activation of the classical pathway of complement in vitro since serum drawn from these patients at 37 degrees C lost hemolytic activity in 4 hours when transferred to a cold environment. Neither HB antigen nor cryoglobulin participated in this phenomenon. The activation of complement in the cold could be prevented by increasing the ionic strength, or by adding vitamin E or, to a lesser extent its vehicle HCO-60, while heparin, Trasylol, soybean trypsin inhibitor, or hirudin had no effect. Trans-AMCHA prevented activation in one case. It is speculated that a factor appearing as a result of blood clotting is able to activate the classical pathway of complement in the cold; it is probably not related to Hageman factor (factor XII), factor VII, thrombin, kallikrein.
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PMID:Cold activation of complement i. presence of coagulation-related activator. 5 81

We have evaluated the influence of NBT, vitamin E, and the combination of NBT and vitamin E on the fine structure and biochemistry of platelets during incubation, and the effects of these compounds on the aggregation and secretion of platelets stimulated by collagen, thrombin, epinephrine, and ADP. Results demonstrate that NBT and vitamin E, rather than injuring platelets, appear to protect them during incubation. Togheter NBT and vitamin E blockedaggregation by epinephrine, collagen, and thrombin, but permitted a small first wave stimulated by ADP. This pattern of response to aggregating agents was similar to reactions observed in platelets pretreated with aspirin and indomethacin, both potent inhibitors of platelet prostaglandin synthesis. The findings support the concept that conversion of arachidonic acid to an activated state is an important step in prostaglandin synthesis and that electron transfer or oxidation--reduction reactions are intimately involved in the development of platelet stickiness. Although vitamin E alone does not block prot to regulate formation of endoperoxides and thromboxanes.
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PMID:Vitamin E and platelets: cooperative interactions with nitroblue tetrazolium on inhibition of adhesion, aggregation and secretion. 39 98

All agents capable of triggering the platelet release reaction also stimulate prostaglandin biosynthesis in these cells. Information concerning the endoperoxides, thromboxanes, and more stable metabolites generated by the action of cyclooxygenase and lipoxygenase on arachidonic acid has accumulated rapidly, but little is known about the preliminary steps in the cleavage and preparation of arachidonic acid for insertion into the enzymatic pathways of prostaglandin synthesis. Studies in this laboratory have shown that the combination of nitroblue tetrazolium (NBT) and vitamin E which prevents oxygenation of arachidonic acid to a free radical also blocks platelet prostaglandin biosynthesis. The present study has evaluated the influence of NBT, vitamin E, and the combination of NBT and vitamin E on the fine structure and biochemistry of platelets during incubation, and the effects of these compounds on the aggregation and secretion of platelets stimulated by collagen, thrombin, epinephrine, and ADP. Results of the study demonstrate that NBT and vitamin E, rather than injuring platelets, appear to protect them during incubation. Together NBT and vitamin E blocked aggregation by epinephrine, collagen, and thrombin, but permitted a small first wave stimulated by ADP. Both ADP and thrombin induced shape change, pseudopod formation, and limited degrees of internal contraction in vitamin E-NBT-treated platelets, whereas epinephrine and collagen failed to significantly alter discoid form. This pattern of response to aggregating agents was identical to reactions observed in platelets pretreated with aspirin and indomethacin, both potent inhibitors of platelet prostaglandin synthesis. In addition, NBT-vitamin E virtually blocked the first wave of aggregation which is not affected by aspirin and indomethacin. The findings support the concept that conversion of arachidonic acid to an activated state is an important step in prostaglandin synthesis and that electron transfer or oxidation-reduction reactions are intimately involved in the development of platelet stickiness.
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PMID:Effects of nitroblue tetrazolium and vitamin E on platelet ultrastructure, aggregation, and secretion. 87 76

In the present study performed on rats, we investigated the influence of an in vivo acute iron load on several platelet parameters and their modification after vitamin E supplementation. Iron load was achieved by injecting iron dextran corresponding to 0.1 mg Fe3+ per kg in the gluteus muscles. Control rats were injected with an equal amount of a dextran solution. Analyses were performed 18 h after injection. By comparison with controls, in iron-injected animals, we found significant increases of: (1) serum total iron (by 110%); (2) aggregation of isolated platelets induced by low concentration of thrombin and ADP (by 350% and 120%, respectively); (3) thrombin-induced endogenous serotonin secretion (by 94%). We also studied the mobilization of radiolabeled arachidonate preincorporated into platelet phospholipids. The results indicated that the thrombin-stimulated release of arachidonate and formation of cyclooxygenase and lipoxygenase products (particularly thromboxane B2), were significantly increased. We also found in plasma an increase (by 67%) of malondialdehyde (MDA) as well as a decrease of vitamin E (by 60%). When vitamin E was injected the day before iron injection, platelet hyperactivity and thromboxane biosynthesis were reduced as well as the plasma MDA concentration. Consequently, given the key role of calcium flux in the activation processes in platelets, we also investigated the thrombin-induced Ca2+ uptake by means of radiocalcium. We found that in platelets from iron-treated rats the Ca2+ uptake amounted to 3670 +/- 201 pmol/10(9) platelets (plt) and was significantly different from controls (1680 +/- 192 pmol/10(9) plt, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of vitamin E on acute iron load-potentiated aggregation, secretion, calcium uptake and thromboxane biosynthesis in rat platelets. 146 49

The effects of vitamin E and D-myo-inositol 1,2,6-trisphosphate (PP-56) were investigated in long-term studies in streptozocin-induced diabetic rats fed a purified diet with 33% lipids and a polyunsaturated-to -saturated fatty acid ratio of 1. A supplement of vitamin E decreased plasma triglycerides, platelet lipid biosynthesis, some of the delta 6- and delta 5-desaturase abnormalities, and urine ketone bodies but did not affect the response of platelets to aggregation. PP-56 completely normalized the platelet reactivity to ADP and thrombin. This was accompanied by normalization of platelet lipid biosynthesis and diabetes-induced abnormalities in delta 6- and delta 5-desaturases. PP-56 treatment also reduced the mortality rate and to a certain extent urinary ketone bodies. The protective effect of PP-56 on platelet aggregation and mortality rate were dose related. PP-56, a molecule derived from phytic acid, seems to exert potent protective effects on some of the manifestations associated with diabetes in rats.
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PMID:Effects of PP-56 and vitamin E on platelet hyperaggregability, fatty acid abnormalities, and clinical manifestations in streptozocin-induced diabetic rats. 182 73

The bioactivities of RRR-alpha-, beta-, gamma-, and delta-tocopherol (T) and R-alpha-tocotrienol (R-alpha-TT) were determined in rat resorption-gestation tests. The ranking order was RRR-alpha-T greater than RRR-beta-T greater than RRR-gamma-T greater than or equal to R-alpha-TT greater than RRE-delta-T. Accordingly, the biopotency of a palm-oil residue was assessed and expressed as alpha-tocopherol equivalents (alpha-TEs). The release of pyruvate kinase, a variable in the nutrition-linked necrotizing myopathy, into the plasma was dose-dependently inhibited by the RRR-alpha-T standard and the corresponding alpha-TE from this residue. Prostacyclin synthesis from aorta segments induced by thrombin or ionomycin was higher than the spontaneous release. However, there was no difference between the depleted group and groups treated with RRR-alpha-T or alpha-TEs from the palm-oil residue. Quantities of IgG in plasma of vitamin E-depleted rats were the highest. Upon supplementation with RRR-alpha-T or alpha-TEs from the palm-oil residue, reduced IgG concentrations were observed, similar to those of animals on a commercial diet containing adequate amounts of vitamin E.
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PMID:Functions of vitamin E in reproduction and in prostacyclin and immunoglobulin synthesis in rats. 201 18

Male Fisher rats were fed chow diets for two weeks after which they were divided into seven groups of ten rats each and fed 20% Canola, 20% menhaden, 20% partially hydrogenated soy oil (PHSO) or chow only, with or without 500 mg/Kg dietary vitamin E in chow containing 2% cholesterol for six weeks. Triglycerides were lower in the menhaden group and were essentially the same in the E supplemented groups as in their unsupplemented cohorts. Plasma cholesterol was higher in the Canola, and lower in the menhaden, groups, compared to the PHSO group. Cholesterol was the same in the E supplemented groups as in their unsupplemented cohorts. Plasma thiobarbituric acid reactant substances (TBARS) were higher in the menhaden group, compared to the chow group. Vitamin E supplementation lowered TBARS in the menhaden and PHSO groups, compared to the unsupplemented cohorts. Collagen induced platelet aggregation was lower in both Canola and menhaden groups, compared to the PHSO group. Vitamin E supplementation lowered collagen induced platelet aggregation only in the PHSO group. Thrombin induced platelet aggregation was lower in the Canola group, compared to the PHSO group. Vitamin E supplementation did not affect thrombin induced platelet aggregation compared to unsupplemented cohorts. Plasma vitamin E levels were lowest in the menhaden supplemented group compared to all other groups not receiving E, suggesting a greater requirement for E in this group. Finally, vitamin E supplementation raised the plasma E levels in all groups except the menhaden group when compared to unsupplemented cohorts.
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PMID:Effect of dietary menhaden, Canola and partially hydrogenated soy oil supplemented with vitamin E upon plasma lipids and platelet aggregation. 202 42

Elderly people present an increased incidence of atherosclerosis and vascular cerebral damages, associated with blood platelet hyperactivity and a stimulation of arachidonic acid metabolism in vivo. The effects of a low intake of purified eicosapentaenoic acid (EPA) on platelet hyperactivity in old human subjects has been investigated. In a randomized, double blind study, 8 people took during 2 months a daily intake of 100 mg of eicosapentaenoic acid (EPA) given as a triglyceride (1,3-dioctanoyl,2-eicosapentaenoyl-glycerol), and 8 other subjects ingested a placebo. A slight, but significant reduction of platelet-rich plasma aggregation in response to epinephrine and arachidonic acid occurred after EPA intake, as well as a decreased aggregation of washed platelets induced by thrombin, although collagen- and U-46619-induced aggregations were not significantly modified. EPA intake failed to affect arachidonic acid metabolism in thrombin-stimulated platelets or in clotted venous blood. The urinary excretion of thromboxane, 6-keto-PGF1 alpha and their 2,3-dinor-metabolites was also not modified. Similarly, no change in the plasma and platelet lipid fatty acid compositions could be observed. Platelet, but not plasma, alpha- and gamma-tocopherol were enhanced by EPA intake. An increase of platelet vitamin E has been associated with a decrease of aggregation, especially in vitamin E-deficient subjects, like elderly people. Therefore, low intake of EPA might have contributed to inhibit platelet aggregation by increasing cellular vitamin E.
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PMID:Functions and tocopherol content of blood platelets from elderly people after low intake of purified eicosapentaenoic acid. 210 38

We investigated whether changes in plasma oxidative properties could occur after oral (hormonal) contraceptive (OC) administration in female rats and whether such changes could be responsible for the platelet increase in aggregation and lipid biosynthesis observed with that treatment. Platelets and plasma (platelet-poor) from control and OC (ethinyl estradiol + lynestrenol)-treated rats were prepared separately. Thrombin-induced aggregation of control platelets was markedly enhanced after incubation for 4 (p less than 0.025) to 60 (p less than 0.001) minutes in OC as compared with control plasma. Under the same conditions, platelet lipid biosynthesis was increased also (p less than 0.05 to p less than 0.01), but after 3 hours incubation. The enhanced response of platelets to aggregation induced by OC plasma could be inhibited by adding either glutathione (p less than 0.025), vitamin E (p less than 0.025), catalase (p less than 0.05), or peroxidase + glutathione (p less than 0.005) to plasma or 2,6,di-bis(ter-butyl)p-cresol (p less than 0.05) to platelets before incubation. The peroxidized free fatty acids isolated from OC plasma added to normal platelets induced a 150% (p less than 0.001) increase in the response to thrombin as compared with the fatty acids from control plasma. In addition, the level of malondialdehyde and conjugated dienes was significantly (p less than 0.02 to p less than 0.001) increased in OC compared with control plasma. We conclude that the enhanced formation in plasma of lipid hydroperoxides seems to be the initial event stimulating platelets after OC treatment, at least in rats.
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PMID:Hormonal contraceptive increases plasma lipid peroxides in female rats. Relationship to platelet aggregation and lipid biosynthesis. 253 71

A randomized, placebo-controlled double-blind trial was conducted on 20 adults to assess the effect of vitamin E (800 IU/d 727 mg/d for 5 wk) on platelet function, arachidonic acid metabolism, and prostacyclin generation. Platelet aggregation was measured in response to collagen, arachidonic acid, and adenosine diphosphate. Thromboxane B2 was assayed in serum and in the supernatant plasma after platelet aggregation. Platelets were labeled with [3H]arachidonic acid to assess production and release of cyclooxygenase products (MDA, TXB2, and HHT), a lipoxygenase product (12-HETE), and arachidonic acid in response to stimulation by thrombin or collagen. Prostacyclin was measured in plasma and in blood collected from bleeding-time incisions by a sensitive HPLC-RIA procedure. Despite marked increases in plasma and erythrocyte vitamin E levels in the vitamin E group, there were no significant differences between the vitamin E and placebo groups in any of the variables measured.
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PMID:Vitamin E supplementation effect on human platelet function, arachidonic acid metabolism, and plasma prostacyclin levels. 312


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