Enzymes that hydrolyze adenine nucleotides in patients with ischemic heart disease.

BACKGROUND: The extracellular nucleotides, ATP and ADP, as well as the nucleoside adenosine have been implicated in a great number of pathologic and physiological functions. However, extracellular adenine nucleotide levels are controlled by a complex cell surface-located group of enzymes called ectonucleotidases. We evaluated activities of enzymes that hydrolyze adenine nucleotides and nucleosides in platelets from patients with ischemic heart disease (IHD). METHODS: Sixty IHD patients were selected for the study. The activities of ectonucleoside triphosphate diphosphohydrolase (NTPDase, CD39), ectonucleotide pyrophosphatase/phosphodiesterase (E-NPP), ecto-5'-nucleotidase and adenosine deaminase (ADA) were studied in isolated platelets of these patients, as well as the platelet aggregation and NTPDase expression. RESULTS: The results show that NTPDase, ecto-5'-nucleotidase, E-NPP activities and NTPDase expression were increased in platelets of IHD patients when compared with the control group (p < 0.05). On the other hand, ADA activity and platelet aggregation were decreased in IHD patients, when compared with the control group (p < 0.05). CONCLUSIONS: The pathological condition in IHD generates alterations in ectonucleotidase activities as a compensatory organic response to thrombotic events that occur in IHD.

Oxidative stress versus antioxidant defenses in patients with acute myocardial infarction.

Acute myocardial infarction (AMI) is a highly dynamic event, which is associated with increasing production of reactive oxygen species (ROS). The imbalance between ROS production and antioxidant defenses leads to the condition known as oxidative stress. The most widely recognized effect of increasing oxidative stress is the oxidation and damage of macromolecules, membranes, proteins, and DNA. Therefore, in this study we sought to evaluate oxidative stress and antioxidant defenses in patients with AMI. Lipid peroxidation, protein carbonyl levels, and enzymatic and nonenzymatic antioxidants were assessed in samples obtained from 40 AMI patients and 40 control patients. AMI was characterized by clinical, electrocardiographic, and laboratory criteria. The control group was divided into two groups of 20 patients: a control group with healthy patients and a risk group. Our results demonstrated an increase in substances reactive to thiobarbituric acid (TBARS) and carbonyl protein levels in the AMI and risk groups. In addition, a positive correlation was found between TBARS, carbonyl protein levels, and troponin I in AMI patients. Surprisingly, for the enzymatic antioxidant defenses, catalase and superoxide dismutase, we observed an increase in these parameters in the AMI and risk groups when compared with healthy patients. However, a decrease in nonenzymatic antioxidants such as vitamin C and vitamin E was observed in AMI patients when compared with the healthy group and the risk group. The increase in oxidative stress was probably a result of the elevation in ROS production due to the ischemic/reperfusion event that occurs in AMI, in addition to the decrease of nonenzymatic antioxidant defenses.

Hydrolysis of adenine nucleotides in platelets from patients with acute myocardial infarction.

OBJECTIVES: To investigate the rate of ATP, ADP and AMP hydrolysis on the surface of platelets from acute myocardial infarction (AMI) patients. DESIGN AND METHODS: Twenty-five patients diagnosed with AMI, through clinical criteria, electrocardiographic changes and increase of cardiac biomarkers, as well as 25 healthy patients were selected. The hydrolysis of ATP, ADP and AMP was verified in isolated platelets of these patients. RESULTS: The results demonstrated that an increase in ATP (54%) and ADP (45%) hydrolysis occurred in AMI patients when compared to the control group. The hydrolysis of AMP also increased by 46% in AMI patients probably leading to an enhancement in the adenosine level. CONCLUSIONS: Our results suggest an increase in nucleotide hydrolysis in platelets from AMI patients, which could be related to a compensatory organic response to thrombotic events that occur in AMI.