Maísa de Carvalho Corrêa

Diet-Induced Changes in AChE Activity after Long-Term Exposure

In the present study we investigated a potential mechanism by which high sugar (HS) and high fat (HF) diets could affect acetylcholinesterase (AChE) activity. The treatment with HS and HF diet was done for six months on male and female rats. The results showed decreased hippocampal AChE activity in male and females receiving HS and HF diets (HS 24% and 36%; HF 38% and 32%, males and females, respectively; P < 0.05). The activity in the cerebral cortex was reduced in males (49 and 40%) and females (19 and 17%) (P < 0.05) on HS and HF diets, respectively. In the hypothalamus AChE activity was decreased on HS diet in males (46%) and female (25%) (P < 0.05) and also on HF diet in males (34%) and females (21%) (P < 0.05). However, in the cerebellum no changes in AChE activity were observed. These results indicate that HS and HF diets produced mainly inhibition in acetylcholine degradation. It probably indicates a chronic alteration induced by these diets on the cholinergic system.

Changes in acetylcholinesterase (AchE) activity in lymphocytes and whole blood in acute lymphoblastic leukemia patients

BACKGROUND Acute lymphoblastic leukemia (ALL) is a type of cancer that affects lymphocytes and it is the most common form of cancer in children. Acetylcholinesterase (AChE) is well known as having non-cholinergic functions and has been detected in the blood and plasma of humans including in lymphocytes. Thus, we investigated whole blood and lymphocyte AChE activity in patients with ALL. METHODS This study was performed on 72 children with ALL divided into 4 groups: newly diagnosed, remission induction, remission maintenance and out-of-treatment and one control group of 50 healthy subjects. We determined AChE activity in whole blood and lymphocytes of these patients. RESULTS Results demonstrated that whole blood AChE activity was enhanced in the newly diagnosed group and reduced in the remission induction and remission maintenance groups in relation to the control group. For lymphocyte AChE activity we found an increase in the newly diagnosed group and a decrease in the remission induction group in relation to the control. CONCLUSIONS These results suggest that AChE activity was altered in ALL patients. This fact may be related with the essential role played by AChE in the development of hematological disease and its contribution to the regulation of immune function.

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.

Lipid peroxidation in rats treated with vincristine sulphate and nandrolone decanoate

Brain and serum lipid peroxidation was studied in rats treated with vincristine sulphate and different doses of nandrolone decanoate. Thirty rats were distributed into six groups (n=5). The treatments were applied once a week for two weeks. Sample collection was performed in the third week. Treatments during the first week were: G1 (control) - physiologic solution, G2 - vincristine sulphate (4mg/m2), G3 - physiologic solution, G4 - physiologic solution, G5- vincristine sulphate (4mg/m2), and G6 - vincristine sulphate (4mg/m2). In the second week, they were: G1 (control) - physiologic solution, G2- physiologic solution, G3 - nandrolone decanoate (1.8mg/kg-1), G4 - nandrolone decanoate (10mg/kg-1), G5 - nandrolone decanoate (1.8mg/kg-1), and G6 - nandrolone decanoate (10mg/kg-1). Lipid peroxidation increased with the isolated use of vincristine and nandrolone decanoate, and with vincristine associated to the highest dose of the ester as well. These results suggest that vincristine sulphate and nandrolone decanoate increase free radical production. Therapeutic dose of nandrolone decanoate when associated with vincristine sulphate proved to be beneficial, as it was able to protect the organism from damaging processes involved in free radical production

ORAL ADMINISTRATION OF N-ACETYLCYSTEINE IMPROVES BIOCHEMICAL PARAMETERS IN DIABETIC RATS

To evaluate the effect of N-acetylcysteine (NAC), a potent ROS scavenger and thiol group supplier, on normoglycemic and diabetic rats, the animals received 50 or 200 mg/kg NAC by gavage daily for 45 days. The results showed a lack of uniformity in acetylcholinesterase activity among the four cerebral structures. While neither dose of NAC produced significant hypoglycemic activity, 50 mg/kg NAC partially reverted the weight loss of diabetics and was effective in restoring aminolevulinate dehydratase activity and non-protein thiol content in liver, and in diminishing serum protein carbonylation. The dose of 200 mg/kg NAC presented some negative effects per se in both the antioxidant and cholinergic systems. In conclusion, 50 mg/kg NAC produced an improvement in some parameters suggesting NAC as a possible drug in antioxidant therapies against diabetic state. However, future studies are necessary to investigate the better dose of this compound to counteract its undesirable effects.