Activity of cholinesterases and adenosine deaminase in blood and serum of rats experimentally infected with Trypanosoma cruzi.

This study aimed to evaluate the activity of cholinesterases and adenosine deaminase (ADA) in blood and serum of rats infected with Trypanosoma cruzi. Twelve adult rats were used in the experiment divided into two uniform groups. Rodents from group A (control group) were non-infected and animals from group B served as infected, receiving intraperitoneally 3·3×10(7) trypomastigotes/each. Blood collection was performed at days 60 and 120 post-infection (PI) in order to evaluate the hemogram, blood activity of acetylcholinesterase, and serum butyrylcholinesterase and ADA activities. Hematological parameters did not differ between groups. A significant increase (P<0·05) of acetylcholinesterase activity was observed in blood while butyrylcholinesterase had a significant reduction (P<0·01) in serum of infected rats at days 60 and 120 PI. ADA activity in serum showed an inhibition in infected animals when compared to non-infected at day 120 PI. Based on these results, it is possible to conclude that the activity of cholinesterases and ADA were changed in animals infected with T. cruzi. The possible causes of these alterations will be discussed in this paper.

Hypoxic-ischemic brain injury stimulates inflammatory response and enzymatic activities in the hippocampus of neonatal rats.

Brain damage from neonatal hypoxia-ischemia (HI) plays a major role in neonatal mortality and morbidity. Using the Rice-Vannucci model of HI in rats, we verified that 8 days after HI injury, adenosine deaminase (ADA), N-acetyl-glucosaminidase (NAG) and myeloperoxidase (MPO) activities increased in the left hemisphere hippocampus (HI group); however, the activity of 5'-nucleotidase (5'NT) remained unchanged. In the hematoxylin-eosin analysis (HE), we detected selective and delayed degeneration of hippocampal pyramidal neurons and astroglial reaction accompanied by glial fibrillary acidic protein (GFAP)-positive and vimentin-positive in the immunohistochemistry analysis in the HI group compared with the control group. We observed the selective necrosis of neurons, vascular endothelial proliferation and inflammatory response accompanied by the increase of the key enzyme of adenosine metabolism in the HI group. The increase of ADA activity, despite the 5'NT activity was not altered, indicates the predominance of ADA activity in the postischemic homeostasis of extra cellular adenosine. The presence of leukocytes into the ischemic areas displays the possible importance of the neutrophil-macrophages associated with the increase of MPO and NAG activities 8 days after HI. These findings may contribute to the evaluation of some consequences of the damage caused by neonatal HI.

Assessment of uric acid and lipid peroxidation in serum and urine after hypoxia-ischemia neonatal in rats.

The aim of this study was to evaluate urinary uric acid (UA) and lipid peroxidation levels, plasma myeloperoxidase (MPO) and adenosine deaminase (ADA) activities, and serum UA in neonatal rats subjected to hypoxia-ischemia neonatal HI model. The relevance of the findings is the fact that urinary lipid peroxidation and UA levels were significantly higher in 8 days in HI group when compared with the control, returning to baseline levels 60 days after HI. Hence, being an indication of purinic degradation during these first days post-HI. Furthermore, the higher levels of malondialdehyde (MDA) in urine in this period may be related to inadequate scavenging abilities of the immature nervous system and being noninvasive it may suggest the use of urinary MDA measurement as a marker for lipid peroxidation after HI insult. In application terms, these findings can help develop therapeutic interventions as soon as 8 days after HI.

Evaluation of cerebrospinal fluid adenosine deaminase activity in HIV-seropositive subjects and its association with lactate dehydrogenase and protein levels.

The purpose of this study was to investigate the role of ADA as additional marker of HIV infection as well as its association with other biochemical markers. This study included 55 patients, 26 being diagnosed as HIV positive and 29 patients diagnosed as HIV negative. Glucose, total protein, lactate dehydrogenase, and adenosine deaminase (ADA) activity were measured on cerebrospinal fluid (CSF). ADA activity on CSF was statistically different in HIV-seropositive subjects compared with HIV-negative subjects. The sensitivity and specificity of ADA activity on CSF was 50 and 82.76%, respectively. ADA activity was positively correlated with lactate dehydrogenase and protein in patients with HIV positive and it was negatively correlated with glucose levels. ADA determination in CSF could add information about inflammatory processes in patients with HIV infection.

Decrease of adenosine deaminase activity and increase of the lipid peroxidation after acute methotrexate treatment in young rats: protective effects of grape seed extract.

The methotrexate (MTX) is an anti-folate used to treat cancer and some inflammatory diseases. The efficacy of MTX is often limited by its severe toxicity. The present study was undertaken to determine whether Grape seed (Cabernet Sauvignon) extract (GSE) could ameliorate the MTX-induced oxidative injury and the effect on adenosine deaminase activity (ADA) in rats. The rats were pretreated with 50 mg/kg of GSE, i.p., prior to MTX administration (10 mg/kg, i.p.) with a second dose given 4 h and a third dose 16 h after MTX administration. Biochemical parameters were investigated 48 h after the last MTX administration. The administration of MTX increased thiobarbituric acid reactive species (TBARS) levels in hippocampus, kidney and liver, whereas induced a significant decreased in the ADA activity in the cerebral cortex, kidney and liver tissues. MTX administration significantly increased the activity of ALT(alanine aminotransferase) and urea levels and decreased uric acid levels in the serum. Urinary uric acid levels decreased in the MTX group when compared to those of the control group. The GSE along with MTX-administration significantly reversed these parameters toward to near normal. These results indicated that GSE could reduce hepatic and nephritic damage induced by MTX-treatment in young rats therefore having free radical scavenging.

Adenosine deaminase activity, lipid peroxidation and astrocyte responses in the cerebral cortex of rats after neonatal hypoxia ischemia.

Hypoxia ischemia (HI) is a common cause of damage in the fetal and neonatal brain. Lifelong disabilities such as cerebral palsy, epilepsy, behavioral and learning disorders are some of the consequences of brain injury acquired in the perinatal periods. Inflammation and formation of free radicals appear to play key roles in neonatal HI. The aim of this study was to describe the chronological sequence of adenosine deaminase (ADA) activity, the oxidative damage changes and astrocyte response using the classic model of neonatal HI. We observed an increase in the activity of ADA and lipid peroxidation in the cerebral cortex 8 days after neonatal HI. This was accompanied by a GFAP-positive, and the degree of brain damage was determined histochemically by hematoxylin-eosin (HE). Taking into account the important anti-inflammatory role of adenosine, ADA may provide an efficient means for scavenging cell-surrounding adenosine and play an important part in subsequent events of neonatal HI in association with GFAP reactive gliosis. The present investigation showed that neonatal HI causes the increase of free radicals and significant damage in the cerebral cortex. The increase in ADA activity may reflect the activation of the immune system caused by HI because the morphological analysis exhibited a lymphocytic infiltration.