Lara Vargas Becker

Ectonucleotide Pyrophosphatase/Phosphodiesterase (E-NPP) and Adenosine Deaminase (ADA) activities in patients with uterine cervix neoplasia

OBJECTIVE Ectonucleotide pyrophosphatase/phosphodiesterase (E-NPP) and adenosine deaminase (ADA) activities, in the platelets and serum, were examined in patients with uterine cervix neoplasia without treatment as well as in patients treated by conization or radiotherapy (RTX). DESIGN AND METHODS The patients were divided based on the amount of time from the end of the treatments until the day of the blood sampling. Groups I (n=19) (conization) and III (n=11) (radiotherapy) (treated from one to five years earlier), groups II (n=19) (conization) and IV (n=16) (radiotherapy) (treated recently; up to three months earlier) and the non-treated group (cancer) (n=7). RESULTS E-NPP and ADA in the platelets and E-NPP in the serum were decreased in all the treated groups in relation to the control and non-treated groups, while ADA in the serum was decreased only in the conization groups in relation to them. In group II, E-NPP and ADA, in the platelets, were increased in relation to group IV. CONCLUSION The tendency of reduction for E-NPP and ADA indicates that they may act together to control nucleotide levels and it may also be speculated that surgery causes greater platelet activation contributing to the changes seen in the conization groups. In this sense, platelets seem to be more sensitive than serum.

The effect of aluminium on NTPDase and 5′-nucleotidase activities from rat synaptosomes and platelets

Aluminium (Al), a neurotoxic compound, has been investigated in a large number of studies both in vivo and in vitro. In this study, we investigated the effect in vivo of long‐term exposure to Al on NTPDase (nucleoside triphosphate diphosphohydrolase) and 5′‐nucleotidase activities in the synaptosomes (obtained from the cerebral cortex and hippocampus) and platelets of rats. Here, we investigated a possible role of platelets as peripheral markers in rats. Rats were loaded by gavage with AlCl3 50 mg/(kg day), 5 days per week, totalizing 60 administrations. The animals were divided into four groups: (1) control (C), (2) 50 mg/kg of citrate solution (Ci), (3) 50 mg/kg of Al plus citrate (Al + Ci) solution and (4) 50 mg/kg of Al (Al). ATP hydrolysis was increased in the synaptosomes from the cerebral cortex by 42.9% for Al + Ci and 39.39% for Al, when compared to their respective control (p < 0.05). ADP hydrolysis was increased by 13.15% for both Al and Al + Ci, and AMP hydrolysis increased by 32.7% for Al and 27.25% for Al + Ci (p < 0.05). In hippocampal synaptosomes, the hydrolysis of ATP, ADP and AMP, was increased by 58.5%, 28.5% and 25.92%, respectively, for Al (p < 0.05) and 36.7%, 22.5% and 37.64% for Al + Ci, both when compared to their respective controls. ATP, ADP and AMP hydrolysis, in platelets, was increased by 172.3%, 188.52% and 92.1%, respectively in Al + Ci, and 317.9%, 342.8% and 177.9%, respectively, for Al, when compared to their respective controls (p < 0.05). Together, these results indicate that Al increases NTPDase and 5′‐nucleotidase activities, in synaptosomal fractions and platelets. Thus, we suggest that platelets could be sensitive peripheral markers of Al toxicity of the central nervous system.

Activities of enzymes that hydrolyze adenine nucleotides in lymphocytes from patients with rheumatoid arthritis.

The purpose of this study was to investigate the activities of ecto‐nucleoside triphosphate diphosphohydrolase (E‐NTPDase; EC 3.6.1.5; CD39) and adenosine deaminase (E‐ADA; EC 3.5.4.4) in lymphocytes from patients with rheumatoid arthritis (RA). Thirty patients diagnosed with RA through American College of Rheumatology criteria as well as 30 healthy patients were selected. Peripheral blood lymphocytes were isolated, and E‐NTPDase and E‐ADA activities were assayed. The results demonstrated an increased E‐NTPDase activity (both ATP and ADP as substrates) and a decreased E‐ADA activity in RA patients. These data suggest an organic effort to preserve the adenosine level, which is known to have anti‐inflammatory and analgesic properties, working as a potent suppressor of immune response. Copyright

NTPDase and 5′-nucleotidase activities from synaptosomes and platelets of rats exposed to cadmium and treated with N-acetylcysteine

The purpose of the present investigation was to evaluate the hydrolysis of adenine nucleotides on synaptosomes and platelets obtained from rats exposed to cadmium (Cd) and treated with N‐acetylcysteine (NAC). Rats received Cd (2 mg/kg) and NAC (150 mg/kg) by gavage every other day for 30 days. Animals were divided into four groups (n = 4–6): control/saline, NAC, Cd, and Cd/NAC. The results of this study demonstrated that NTPDase and 5′‐nucleotidase activities were increased in the cerebral cortex synaptosomes of Cd‐poisoned rats, and NAC co‐treatment reversed these activities to the control levels. In relation to hippocampus synaptosomes, no differences on the NTPDase and 5′‐nucleotidase activities of Cd‐poisoned rats were observed and only the 5′‐nucleotidase activity was increased by the administration of NAC per se. In platelets, Cd‐intoxicated rats showed a decreased NTPDase activity and no difference in the 5′‐nucleotidase activity; NAC co‐treatment was inefficient in counteracting this undesirable effect. Our findings reveal that adenine nucleotide hydrolysis in synaptosomes and platelets of rats were altered after Cd exposure leading to a compensatory response in the central nervous system and acting as a modulator of the platelet activity. NAC was able to modulate the purinergic system which is interesting since the regulation of these enzymes could have potential therapeutic importance. Thus, our results reinforce the importance of the study of the ecto‐nucleotidases pathway in poisoning conditions and highlight the possibility of using antioxidants such as NAC as adjuvant against toxicological conditions.