Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.3.5 (5'-nucleotidase)
 3,167 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperhomocysteinemia is an independent risk factor for atherothrombotic disease. Platelets play an important role in cardiovascular disease and release pro-aggregates mediators when activated, such as ADP, a physiological agonist involved in normal hemostasis and thrombosis. NTPDases and 5'-nucleotidase are ecto-enzymes that hydrolyze ATP, ADP and AMP to adenosine playing an important role on blood flow and thrombogenesis by regulating ADP catabolism. The aim of the present study was evaluate extracellular adenine nucleotide hydrolysis of rat platelets exposed to homocysteine in vitro and in vivo. In vitro homocysteine (Hcy) in the concentration range of 20 to 500 microM caused a significant decrease on ATP (around 30%) and ADP (around 45%) hydrolysis, respectively, while AMP hydrolysis was not altered. Hcy was not able to inhibit the hydrolysis of ATP and ADP catalyzed by purified apyrase at the same concentrations tested in vitro on platelets, suggesting an indirect effect. The inhibitory effect of Hcy on platelets was prevented by antioxidants agents in vitro and in vivo. Furthermore homocysteine treatment increased platelet aggregation induced by ADP. Based on the results presented herein, we propose that inhibition of extracellular ATP and ADP hydrolysis caused by homocysteine was probably due oxidative stress, since antioxidants prevented such effects. These findings may contribute to an increase platelet response to ADP and consequence development of thrombotic risk attributed to hyperhomocysteinemia.
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PMID:Homocysteine decreases extracellular nucleotide hydrolysis in rat platelets. 1985 Mar 26

Influence of DL-homocysteine thiolactone loading (100 mg/kg by intragastric administration for 28 days) on enzymes activity of adenylic nucleotide and adenosine metabolism in the blood serum, platelets and liver of rats was investigated. The relation between revealed disturbance and platelet hyper-reactivity was estimated. It was established, that apyrase and 5'-nucleotidase activities decreased and adenosine deaminase activity increased in platelets of the rats with hyperhomocysteinemia (HHC). HHC also interrupted adenosine production in the blood serum and liver in rats. Under this condition the platelet sensitivity to ADP-stimulation was significantly increased. Vitamin-microelement complex decreased HHC-induced disorder of adenosine metabolism and prevented platelet hyper-reactivity formation. In vitro homocysteine inhibited platelet hydrolysis of ADP and AMP in a dose-dependent manner and this effect reduced in the presence of hydrogen sulfide donor NaHS.
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PMID:[Effect of thiolactone homocysteine loading on adenosine metabolism in rats: relationship with platelet hyper-reactivity, correction of this metabolism disorders by vitamin-microelement complex]. 2068 46