Atividade da adenosina desaminase, concentração de nucleotídeos e nucleosídeo de adenina em ratos infectados com Trypanosoma evansi

• Ano de defesa: 2011
• Autor(a) principal: Silva, Aleksandro Schafer da
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Santa Maria; BR; Medicina Veterinária; UFSM; Programa de Pós-Graduação em Medicina Veterinária
• Palavras-chave em Português: Trypanosoma evansi; Ratos; Adenosina; Adenosina deaminase; Rats; Adenosine; Adenosine deaminase; CNPQ::CIENCIAS AGRARIAS::MEDICINA VETERINARIA
• Link de acesso: http://repositorio.ufsm.br/handle/1/4058

The purinergic system is known to be an important signaling pathway in different tissues. Among the components of this system have adenosine, a modulator of central nervous, circulatory and immune systems. The concentration of adenosine in the host is controlled by the enzyme adenosine deaminase (ADA), present in tissues, cells and fluids. As a result, the objectives of this study were (1) to determine the ADA activity in Trypanosoma evansi, (2) evaluate the activity of ADA in serum, erythrocytes, lymphocytes and brain of infected rats, and (3) determine the concentration of nucleotides and nucleosides in serum and cerebral cortex of rats infected with T. evansi. In the first study two mice were infected with T. evansi. When these animals showed high parasitemia (±108 parasites/uL) was performed with blood collection and separation of trypomastigotes by DEAE-cellulose column for performing the assays. Spectrometry was performed by the biochemical detection of ADA in the form trypomastigotes of T. evansi. In a second study, we used 39 rats divided into three groups: group A and B (infected) and group C (C1 and C2 control group) Samples of blood and brain samples were collected on day 4 PI (A and C1) and 20 PI (B and C2). From the blood (with anticoagulant) were separated lymphocytes and erythrocytes for measurement of ADA activity, since the serum was obtained from blood samples stored in tubes without anticoagulant. The brain was separated into cerebellum, cerebral cortex, hippocampus and striatum to evaluate the ADA activity in each structure. Decrease of ADA activity in serum and erythrocytes in rats infected with T. evansi when compared not-infected (P<0.05). ADA activity in lymphocytes was decreased at day 4 PI and increased in day 20 PI. There was no difference in ADA activity in the cerebellum. In the cerebral cortex caused a reduction of ADA activity on days 4 and 20 PI. Decrease of ADA activity in hippocampus and striatum in the day 4 and day 20 PI, respectively. In a third study, 24 rats were used, 12 used as a negative control and 12 infected with T. evansi. On day 4 (n = 6 per group) and 20 PI (n = 6 per group) were performed to obtain blood samples of serum and cerebral cortex for analysis. The samples were prepared for quantification of ATP, ADP, AMP and adenosine. This study found increased concentrations of ATP, AMP and adenosine in the brain and serum of rats infected with T. evansi in both periods, except that the levels of adenosine decreased on day 4 PI. The ADP concentration did not change in this study. Therefore, the infection by T. evansi purinergic system components can be changed, may be involved in immune response, in anemia and neurological signs.