Goncalves JF

References (20)

Title : Uncaria tomentosa improves cognition, memory and learning in middle-aged rats - Castilhos_2020_Exp.Gerontol__111016
Author(s) : Castilhos LG , Oliveira JS , Adefegha SA , Manzoni AG , Passos DF , Assmann CE , Silveira LL , Trelles KB , Kronbauer M , Doleski PH , Bremm JM , Braun J , Abdalla FH , Goncalves JF , Andrade CM , Cruz IM , Burger ME , Leal DBR
Ref : Experimental Gerontology , :111016 , 2020
Abstract : Aging accelerates neurodegeneration, while natural and safe neuroprotective agents, such as Uncaria tomentosa, may help to overcome this problem. This study assessed the effects of U. tomentosa extract treatment on the aging process in the brain of Wistar rats. The spatial memory and learning, acetylcholinesterase (AChE) activity, and DNA damage were assessed. Animals of 14months were tested with different doses of U. tomentosa (5mg/kg, 15mg/kg, and 30mg/kg) and with different durations of treatment (one month and one year). In the Morris Water Maze (MWM), the escape latency was significantly (p<0.0001) shorter in rats that received 5mg/kg, 15mg/kg, and 30mg/kg of U. tomentosa for both one month and one year of treatment. There was a significant difference in time spent at the platform zone (p<0.05) of the middle-aged rats treated with U. tomentosa extract for one year when compared to the control rats. The cortex and hippocampus of rats treated with U. tomentosa for one year showed significant (p>0.05) reduction in AChE activity. DNA damage index on cortex was significantly lower (p<0.05) in animals treated with 30mg/kg of U. tomentosa for one month while all the tested doses demonstrated significant (p<0.001) reductions in DNA damage index in animals treated for one year. In conclusion, U. tomentosa may represent a source of phytochemicals that could enhance memory activity, repair DNA damage, and alter AChE activity, thereby providing neuroprotection during the aging process.
ESTHER : Castilhos_2020_Exp.Gerontol__111016
PubMedSearch : Castilhos_2020_Exp.Gerontol__111016
PubMedID: 32628974

Title : Curcumin attenuates memory deficits and the impairment of cholinergic and purinergic signaling in rats chronically exposed to cadmium - da Costa_2017_Environ.Toxicol_32_70
Author(s) : da Costa P , Goncalves JF , Baldissarelli J , Mann TR , Abdalla FH , Fiorenza AM , da Rosa MM , Carvalho FB , Gutierres JM , de Andrade CM , Rubin MA , Schetinger MR , Morsch VM
Ref : Environ Toxicol , 32 :70 , 2017
Abstract : This study investigated the protective effect of curcumin on memory loss and on the alteration of acetylcholinesterase and ectonucleotidases activities in rats exposed chronically to cadmium (Cd). Rats received Cd (1 mg/kg) and curcumin (30, 60, or 90 mg/kg) by oral gavage 5 days a week for 3 months. The animals were divided into eight groups: vehicle (saline/oil), saline/curcumin 30 mg/kg, saline/curcumin 60 mg/kg, saline/curcumin 90 mg/kg, Cd/oil, Cd/curcumin 30 mg/kg, Cd/curcumin 60 mg/kg, and Cd/curcumin 90 mg/kg. Curcumin prevented the decrease in the step-down latency induced by Cd. In cerebral cortex synaptosomes, Cd-exposed rats showed an increase in acetylcholinesterase and NTPDase (ATP and ADP as substrates) activities and a decrease in the 5'-nucleotidase activity. Curcumin was not able to prevent the effect of Cd on acetylcholinesterase activity, but it prevented the effects caused by Cd on NTPDase (ATP and ADP as substrate) and 5'-nucleotidase activities. Increased acetylcholinesterase activity was observed in different brain structures, whole blood and lymphocytes of the Cd-treated group. In addition, Cd increased lipid peroxidation in different brain structures. Higher doses of curcumin were more effective in preventing these effects. These findings show that curcumin prevented the Cd-mediated memory impairment, demonstrating that this compound has a neuroprotective role and is capable of modulating acetylcholinesterase, NTPDase, and 5'-nucleotidase activities. Finally, it highlights the possibility of using curcumin as an adjuvant against toxicological conditions involving Cd exposure. (c) 2015 Wiley Periodicals, Inc. Environ Toxicol 32: 70-83, 2017.
ESTHER : da Costa_2017_Environ.Toxicol_32_70
PubMedSearch : da Costa_2017_Environ.Toxicol_32_70
PubMedID: 26592365

Title : Silicon Reverses Lipid Peroxidation but not Acetylcholinesterase Activity Induced by Long-Term Exposure to Low Aluminum Levels in Rat Brain Regions - Noremberg_2016_Biol.Trace.Elem.Res_169_77
Author(s) : Noremberg S , Bohrer D , Schetinger MR , Bairros AV , Gutierres J , Goncalves JF , Veiga M , Santos FW
Ref : Biol Trace Elem Res , 169 :77 , 2016
Abstract : Aluminum (Al) is the most widely distributed metal in the environment and is extensively used in daily life leading to easy exposure to human beings. Besides not having a recognized physiological role, Al may produce adverse effects through the interaction with the cholinergic system contributing to oxidative stress. The present study evaluated, in similar conditions of parenteral nutrition, whether the reaction of silicon (SiO2) with Al(3+) to form hydroxyaluminosilicates (HAS) reduces its bioavailability and toxicity through intraperitoneal administrations of 0.5 mg Al/kg/day and/or 2 mg Si/kg/day in Wistar rats. Al and Si concentrations were determined in rat brain tissue and serum. Acetylcholinesterase (AChE) activity and lipid peroxidation (LPO) were analyzed in the cerebellum, cortex, hippocampus, striatum, hypothalamus, and blood. An increase in the Al concentration was verified in the Al + Si group in the brain. All the groups demonstrated enhanced Si compared to the control animals. Al(3+) increased LPO measured by thiobarbituric acid reactive substances (TBARS) in cerebellum and hippocampus, whereas SiO2 reduced it when compared with the control group. An increase of AChE activity was observed in the Al-treated group in the cerebellum whereas a decrease of this enzyme activity was observed in the cortex and hippocampus in the Al and Al + Si groups. Al and Si concentrations increased in rat serum; however, no effect was observed in blood TBARS levels and AChE activity. SiO2 showed a protective effect in the hippocampus and cerebellum against cellular damage caused by Al(3+)-induced lipid peroxidation. Thus, SiO2 may be considered an important protector in LPO induced by Al(3+).
ESTHER : Noremberg_2016_Biol.Trace.Elem.Res_169_77
PubMedSearch : Noremberg_2016_Biol.Trace.Elem.Res_169_77
PubMedID: 26050237

Title : Quercetin protects the impairment of memory and anxiogenic-like behavior in rats exposed to cadmium: Possible involvement of the acetylcholinesterase and Na,K-ATPase activities - Abdalla_2014_Physiol.Behav_135C_152
Author(s) : Abdalla FH , Schmatz R , Cardoso AM , Carvalho FB , Baldissarelli J , de Oliveira JS , Rosa MM , Goncalves Nunes MA , Rubin MA , da Cruz IB , Barbisan F , Dressler VL , Pereira LB , Schetinger MR , Morsch VM , Goncalves JF , Mazzanti CM
Ref : Physiol Behav , 135C :152 , 2014
Abstract : The present study investigated the effects of quercetin in the impairment of memory and anxiogenic-like behavior induced by cadmium (Cd) exposure. We also investigated possible alterations in acetylcholinesterase (AChE), Na+,K+-ATPase and delta-aminolevulinate dehydratase (delta-ALA-D) activities as well as in oxidative stress parameters in the CNS. Rats were exposed to Cd (2.5mg/kg) and quercetin (5, 25 or 50mg/kg) by gavage for 45days. Animals were divided into eight groups (n=10-14): saline/control, saline/Querc 5mg/kg, saline/Querc 25mg/kg, saline/Querc 50mg/kg, Cd/ethanol, Cd/Querc 5mg/kg, Cd/Querc 25mg/kg and Cd/Querc 50mg/kg. Results demonstrated that Cd impaired memory has an anxiogenic effect. Quercetin prevented these harmful effects induced by Cd. AChE activity decreased in the cerebral cortex and hippocampus and increased in the hypothalamus of Cd-exposed rats. The Na+,K+-ATPase activity decreased in the cerebral cortex, hippocampus and hypothalamus of Cd-exposed rats. Quercetin prevented these effects in AChE and Na+,K+-ATPase activities. Reactive oxygen species production, thiobarbituric acid reactive substance levels, protein carbonyl content and double-stranded DNA fractions increased in the cerebral cortex, hippocampus and hypothalamus of Cd-exposed rats. Quercetin totally or partially prevents these effects caused by Cd. Total thiols (T-SHs), reduced glutathione (GSH), and reductase glutathione (GR) activities decreased and glutathione S-transferase (GST) activity increased in Cd exposed rats. Co-treatment with quercetin prevented reduction in T-SH, GSH, and GR activities and the rise of GST activity. The present findings show that quercetin prevents alterations in oxidative stress parameters as well as AChE and Na+,K+-ATPase activities, consequently preventing memory impairment and anxiogenic-like behavior displayed by Cd exposure. These results may contribute to a better understanding of the neuroprotective role of quercetin, emphasizing the influence of this flavonoid in the diet for human health, possibly preventing brain injury associated with Cd intoxication.
ESTHER : Abdalla_2014_Physiol.Behav_135C_152
PubMedSearch : Abdalla_2014_Physiol.Behav_135C_152
PubMedID: 24952260

Title : Protective effect of quercetin in ecto-enzymes, cholinesterases, and myeloperoxidase activities in the lymphocytes of rats exposed to cadmium - Abdalla_2014_Mol.Cell.Biochem_396_201
Author(s) : Abdalla FH , Cardoso AM , Schmatz R , Goncalves JF , Baldissarelli J , Martins CC , Zanini D , de Oliveira LS , da Costa P , Pimentel VC , Pereira LB , Lhamas CL , Schetinger MR , Morsch VM , Mazzanti CM
Ref : Molecular & Cellular Biochemistry , 396 :201 , 2014
Abstract : The ex vivo and in vitro effects of quercetin on NTPDase, adenosine deaminase (ADA), and acetycholinesterase (AChE) activities in lymphocytes, as well as the effects of quercetin on butyrylcholinesterase (BChE) activity in serum and myeloperoxidase (MPO) activity in plasma were determined in rats. For the ex vivo experiment, animals were orally exposed to Cadmium (Cd) for 45 days. Animals were divided into eight groups: saline/ethanol, saline/Querc 5 mg/kg, saline/Querc 25 mg/kg, saline/Querc 50 mg/kg, Cd/ethanol, Cd/Querc 5 mg/kg, Cd/Querc 25 mg/kg, and Cd/Querc 50 mg/kg. The ex vivo data showed an increase in the ATP and ADP hydrolysis and ADA activity in Cd-exposed rats when compared to the control group. The treatment with quercetin 25 and 50 mg/kg prevented this increase in the ATP and ADP hydrolysis, while the treatment with quercetin 5, 25, and 50 mg/kg prevented the increase in the ADA activity. AChE, BChE, and MPO activities ex vivo presented an increase in the Cd-exposed group when compared to the control group, and the treatment with quercetin 5, 25, and 50 mg/kg prevented this increase caused by Cd exposure. The in vitro experiment showed that quercetin 5, 10, 25, or 50 microM decreased the ADA activity proportionally to the increase of the concentrations of quercetin when compared to the control group. Thus, we can suggest that the quercetin is able to modulate NTPDase, ADA, AChE, and MPO activities and contribute to maintain the levels of ATP, adenosine, and acetylcholine normal, respectively, exhibiting potent pro-inflammatory and anti-inflammatory actions.
ESTHER : Abdalla_2014_Mol.Cell.Biochem_396_201
PubMedSearch : Abdalla_2014_Mol.Cell.Biochem_396_201
PubMedID: 25064450

Title : Swimming training prevents alterations in acetylcholinesterase and butyrylcholinesterase activities in hypertensive rats - Cardoso_2014_Am.J.Hypertens_27_522
Author(s) : Cardoso AM , Abdalla FH , Bagatini MD , Martins CC , da Silva Fiorin F , Baldissarelli J , Costa P , de Mello FF , Fiorenza AM , da Silva Serres JD , Goncalves JF , Chaves H , Royes LF , Bello-Klein A , Morsch VM , Schetinger MR
Ref : Am J Hypertens , 27 :522 , 2014
Abstract : BACKGROUND: Cholinergic enzyme activities are altered in hypertension, reflecting a low-grade inflammation. Regular physical exercise exerts anti-inflammatory effects and has been described as a coadjutant in the treatment of hypertension. In this study, we investigated the effect of 6 weeks of swimming training on cholinergic enzyme activities (acetylcholinesterase and butyrylcholinesterase) in Nomega-Nitro-L-arginine methyl ester hydrochloride (L-NAME)-induced hypertensive rats.
METHODS: The rats were divided into 4 groups: control (n = 10), exercise (n = 10), L-NAME (n = 10), and exercise L-NAME (n = 10). The animals were trained 5 times per week in an adapted swimming system for 60 minutes with a gradual increase of the workload up to 5% of animal's body weight. Enzyme activities were measured spectrophotometrically in lymphocytes, whole blood, and serum.
RESULTS: A significant rise in acetylcholinesterase activity was observed in lymphocytes and whole blood as well as in serum butyrylcholinesterase activity in the L-NAME group when compared with the other groups (P < 0.05), and the increase in cholinesterase activities was positively correlated with the rise in blood pressure (r = 0.5721, r = 0.6121, and r = 0.5811, respectively). Swimming training was efficient in preventing these alterations in the exercise L-NAME group, which displayed values similar to those of the control group. Exercise training demonstrated a significant hypotensive effect in hypertensive rats.
CONCLUSIONS: Exercise training was shown to prevent increased cholinesterase related to inflammatory processes in hypertensive rats, providing a new insight about protective exercise mechanisms to avoid hypertension-related inflammation.
ESTHER : Cardoso_2014_Am.J.Hypertens_27_522
PubMedSearch : Cardoso_2014_Am.J.Hypertens_27_522
PubMedID: 23479073

Title : Neuroprotective effect of quercetin in ectoenzymes and acetylcholinesterase activities in cerebral cortex synaptosomes of cadmium-exposed rats - Abdalla_2013_Mol.Cell.Biochem_381_1
Author(s) : Abdalla FH , Cardoso AM , Pereira LB , Schmatz R , Goncalves JF , Stefanello N , Fiorenza AM , Gutierres JM , Serres JD , Zanini D , Pimentel VC , Vieira JM , Schetinger MR , Morsch VM , Mazzanti CM
Ref : Molecular & Cellular Biochemistry , 381 :1 , 2013
Abstract : This study investigated the effect of quercetin on nucleoside triphosphate diphosphohydrolase (NTP-Dase), 50-nucleotidase, adenosine deaminase (ADA), and acetylcholinesterase (AChE) activities in synaptosomes from cerebral cortex of adult rats exposed to cadmium (Cd). Rats were exposed to Cd (2.5 mg/Kg) and quercetin (5, 25 or 50 mg/Kg) by gavage for 45 days. Rats were randomly divided into eight groups (n = 8-10): saline/ethanol, saline/Querc 5 mg/kg, saline/Querc 25 mg/kg, saline/Querc 50 mg/kg, Cd/ethanol, Cd/Querc 5 mg/kg, Cd/Querc 25 mg/kg, and Cd/Querc 50 mg/kg. Results demonstrated that AChE activity increased in the Cd/ethanol group when compared to saline/ethanol group. Treatment with quercetin prevented the increase in AChE activity when compared to Cd/ethanol group. Quercetin treatment prevented the cadmium-induced increase in NTPDase, 5-nucleotidase, and ADA activities in Cd/ethanol group when compared to saline/ethanol group. Our data showed that quercetin have a protector effect against Cd intoxication. This way, is a promising candidate among the flavonoids to be investigated as a therapeutic agent to attenuate neurological disorders associated with Cd intoxication.
ESTHER : Abdalla_2013_Mol.Cell.Biochem_381_1
PubMedSearch : Abdalla_2013_Mol.Cell.Biochem_381_1
PubMedID: 23797318

Title : Hematological indices and activity of NTPDase and cholinesterase enzymes in rats exposed to cadmium and treated with N-acetylcysteine - Goncalves_2012_Biometals_25_1195
Author(s) : Goncalves JF , Duarte MM , Fiorenza AM , Spanevello RM , Mazzanti CM , Schmatz R , Bagatini MD , Antes FG , Costa P , Abdalla FH , Dressler VL , Morsch VM , Schetinger MR
Ref : Biometals , 25 :1195 , 2012
Abstract : The present study aimed to investigate the influence of N-acetylcysteine (NAC) on cadmium (Cd) poisoning by evaluating Cd concentration in tissues, hematological indices as well as the activity of NTPDase, acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) enzymes of rats exposed to Cd and co-treated with NAC. For this purpose, the 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 = 6-8): control/saline, NAC, Cd, and Cd/NAC. Cd exposure increased Cd concentration in plasma, spleen and thymus, and NAC co-treatment modulated this augment in both lymphoid organs. Cd exposure reduced red blood cell count, hemoglobin content and hematocrit value. Cd intoxication caused a decrease in total white blood cell count. NAC treatment per se caused an increase in lymphocyte and a decrease in neutrophil counts. On contrary, Cd exposure caused a decrease in lymphocyte and an increase in neutrophil and monocyte counts. NAC reversed or ameliorated the hematological impairments caused by Cd poisoning. There were no significant alterations in the NTPDase activity in lymphocytes of rats treated with Cd and/or NAC. Cd caused a decrease in the activities of lymphocyte AChE, whole blood AChE and serum BChE. However, NAC co-treatment was inefficient in counteracting the negative effect of Cd in the cholinesterase activities. The present investigation provides ex vivo evidence supporting the hypothesis that Cd induces immunotoxicity by interacting with the lymphoid organs, altering hematological parameters and inhibiting peripheral cholinesterase activity. Also, it highlights the possibility to use NAC as adjuvant against toxicological conditions.
ESTHER : Goncalves_2012_Biometals_25_1195
PubMedSearch : Goncalves_2012_Biometals_25_1195
PubMedID: 22991071

Title : Cholinesterase as inflammatory markers in a experimental infection by Trypanosoma evansi in rabbits - Costa_2012_An.Acad.Bras.Cienc_84_1105
Author(s) : Costa MM , Silva AS , Paim FC , Franca R , Dornelles GL , Thome GR , Serres JD , Schmatz R , Spanevello RM , Goncalves JF , Schetinger MR , Mazzanti CM , Lopes ST , Monteiro SG
Ref : An Acad Bras Cienc , 84 :1105 , 2012
Abstract : The aim of this study is to evaluate the role of cholinesterases as an inflammatory marker in acute and chronic infection by Trypanosoma evansi in rabbits experimentally infected. Twelve adult female New Zealand rabbits were used and divided into two groups with 6 animals each: control group (rabbits 1-6) and infected group (rabbits 7-12). Infected group received intraperitoneally 0.5 mL of blood from a rat containing 108 parasites per animal. Blood samples used for cholinesterases evaluation were collected on days 0, 2, 7, 12, 27, 42, 57, 87, 102 and 118 days post-inoculation (PI). Increased activity (P<0.05) of butyrylcholinesterase (BChE) and acetylcholinesterase (AChE) were observed in the blood on days 7 and 27, respectively and no differences were observed in cholinesterase activity in other periods. No significant difference in AChE activity (P>0.05) was observed in the encephalic structures. The increased activities of AChE and BChE probably have a pro-inflammatory purpose, attempting to reduce the concentration of acetylcholine, a neurotransmitter which has an anti-inflammatory property. Therefore, cholinesterase may be inflammatory markers in infection with T. evansi in rabbits.
ESTHER : Costa_2012_An.Acad.Bras.Cienc_84_1105
PubMedSearch : Costa_2012_An.Acad.Bras.Cienc_84_1105
PubMedID: 23011112

Title : Cholinesterases as markers of the inflammatory process in rats infected with Leptospira interrogans serovar Icterohaemorrhagiae - da Silva_2012_J.Med.Microbiol_61_278
Author(s) : da Silva CB , Wolkmer P , Da Silva AS , Paim FC , Tonin AA , Castro VS , Felin DV , Schmatz R , Goncalves JF , Badke MR , Morsch VM , Mazzanti CM , Lopes ST
Ref : J Med Microbiol , 61 :278 , 2012
Abstract : The aim of this study was evaluate changes in the cholinesterase activity in blood, lymphocytes and serum of rats infected with Leptospira interrogans serovar Icterohaemorrhagiae ('L. icterohaemorrhagiae'). Sixty adult Wistar rats were divided into six groups of 10 animals: three control groups and three test groups. The animals from the test groups were intraperitoneally inoculated with 1 ml medium containing 1 x 10(8) leptospires. The activity of acetylcholinesterase in blood and butyrylcholinesterase in serum increased on days 5 (P<0.05) and 30 (P<0.021) post-infection, respectively. A decrease in lymphocyte count was observed on days 15 (P<0.01) and 30 post-infection (P<0.05). On day 15 post-infection, acetylcholinesterase activity (P<0.001) in lymphocytes decreased in infected rats. However, on day 30 post-infection there was an increase in acetylcholinesterase activity in lymphocytes. In conclusion, our results showed that the activity of enzymes of the cholinergic system in the total blood, lymphocytes and serum is altered as a result of inflammation caused by infection with L. icterohaemorrhagiae. The possible causes of these alterations will be discussed in this paper.
ESTHER : da Silva_2012_J.Med.Microbiol_61_278
PubMedSearch : da Silva_2012_J.Med.Microbiol_61_278
PubMedID: 21921108

Title : Acetylcholinesterase activity and lipid peroxidation in the brain and spinal cord of rats infected with Trypanosoma evansi - da Silva_2011_Vet.Parasitol_175_237
Author(s) : Da Silva AS , Monteiro SG , Goncalves JF , Spanevello R , Oliveira CB , Costa MM , Jaques JA , Morsch VM , Schetinger MR , Mazzanti CM , Lopes ST
Ref : Vet Parasitol , 175 :237 , 2011
Abstract : Neurological and locomotor clinical signs are described in animals infected with Trypanosoma evansi. These disturbances may be related to changes in the amount of acetylcholine (neurotransmitter) in the synaptic cleft. Therefore, changes in acetylcholinesterase (AChE) activity and lipid peroxidation in brain and spinal cord of T. evansi-infected rats were investigated. Each rat was intraperitoneally infected with 10(6) trypomastigotes kept in fresh (group A; n=13) and cryopreserved blood (group B; n=13). Thirteen served as uninfected (not-infected; group C). In days 4 and 30 post-infection (PI) the rats were anesthetized and subsequently decapitated to obtain the brain and the spinal cord (between vertebrae L1 and S2). The brain was removed and dissected (cerebellum, cerebral cortex, striatum and hippocampus) to measure the activity of AChE and lipid peroxidation, determined by TBARS levels. To verify if T. evansi was present in the central nervous system (CNS), brain structures of three rats of each group were processed by PCR T. evansi-specific. AChE activity was significantly increased in all brain structures and decrease in spinal cord in infected rats in 4 PI (P<0.05). The levels of TBARS were decreased in the brain structures, differently from spinal cord, which showed increased lipid peroxidation in 4 PI. The AChE activity in striatum, cerebral cortex, hippocampus and spinal cord reduced concomitantly with the increase of the enzyme in cerebellum of the infected rats (P<0.05), and the TBARS levels increased in cerebellum, striatum and spinal cord of infected rats compared to non-infected animals in 30 PI. The PCR was positive for T. evansi in all structures of the brain, confirming the presence of the parasite in the CNS. Based on the results, we conclude that the changes in AChE activity and lipid peroxidation in the CNS are induced by infection with T. evansi, suggesting that the parasite interferes with the cholinergic neurotransmission in this experimental condition.
ESTHER : da Silva_2011_Vet.Parasitol_175_237
PubMedSearch : da Silva_2011_Vet.Parasitol_175_237
PubMedID: 21055876

Title : Trypanosoma evansi: immune response and acetylcholinesterase activity in lymphocytes from infected rats - Da Silva_2011_Exp.Parasitol_127_475
Author(s) : Da Silva AS , Monteiro SG , Goncalves JF , Spanevello R , Schmatz R , Oliveira CB , Costa MM , Franca RT , Jaques JA , Schetinger MR , Mazzanti CM , Lopes ST
Ref : Experimental Parasitology , 127 :475 , 2011
Abstract : The existence of cholinergic receptors in the immune system cells is well documented. This study aimed to evaluate the acetylcholinesterase activity (AChE) in lymphocytes from rats infected with Trypanosoma evansi in acute and chronic phase disease. Twenty animals were infected with 10(6) trypomastigotes forms each and 10 were used as negative controls. The two groups of inoculated rats were formed according to the degree of parasitemia and the period post-infection (PI). Group A: rats with 4 days PI and between 24 and 45 parasites/field (1000x); group B: rats with 30 days PI and parasitemia with jagged peaks between 0 and 1 parasites/field; group C: not-infected animals. At 4 days PI (acute phase) and 30 days PI (chronic phase) the rats were anesthetized to collect blood for hemogram and separation of lymphocytes. After separation, the AChE activity was measured in lymphocytes. It was observed that the number of lymphocytes increased significantly in group A compared to group C. The activity of AChE in lymphocytes significantly increased in acute phase and decreased in chronic phase in the infected rats when compared to not-infected (P<0.05). Statistical analysis showed a positive correlation between the number of lymphocytes and AChE activity in lymphocytes in 4 days PI (r(2): 0.59). Therefore, the infection by T. evansi influences AChE activity in lymphocytes of rats indicating changes in the responses of cholinergic system in acute phase, possibly due to immune functions performed by these enzymes.
ESTHER : Da Silva_2011_Exp.Parasitol_127_475
PubMedSearch : Da Silva_2011_Exp.Parasitol_127_475
PubMedID: 21036170

Title : The effect of curcumin in the ectonucleotidases and acetylcholinesterase activities in synaptosomes from the cerebral cortex of cigarette smoke-exposed rats - Jaques_2011_Cell.Biochem.Funct_29_703
Author(s) : Jaques JA , Rezer JF , Goncalves JF , Spanevello RM , Gutierres JM , Pimentel VC , Thome GR , Morsch VM , Schetinger MR , Leal DB
Ref : Cell Biochemistry & Function , 29 :703 , 2011
Abstract : With the evidence that curcumin may be a potent neuroprotective agent and that cigarette smoke is associated with a decline in the cognitive performance as our bases, we investigated the activities of Ecto-Nucleoside Triphosphate Diphosphohydrolase (NTPDase), 5'-nucleotidase and acetylcholinesterase (AChE) in cerebral cortex synaptosomes from cigarette smoke-exposed rats treated with curcumin (Cur). The experimental procedures entailed two sets of experiments. In the first set, the groups were vehicle, Cur 12.5, 25 and 50 mg.kg(-1) ; those in the second set were vehicle, smoke, smoke and Cur 12.5, 25 and 50 mg.kg(-1) . Curcumin prevented the increased NTPDase, 5'-nucleotidase and AChE activities caused by smoke exposure. We suggest that treatment with Cur was protective because the decrease of ATP and acetylcholine (ACh) concentrations is responsible for cognitive impairment, and both ATP and ACh have key roles in neurotransmission.
ESTHER : Jaques_2011_Cell.Biochem.Funct_29_703
PubMedSearch : Jaques_2011_Cell.Biochem.Funct_29_703
PubMedID: 21932293

Title : N-acetylcysteine prevents memory deficits, the decrease in acetylcholinesterase activity and oxidative stress in rats exposed to cadmium - Goncalves_2010_Chem.Biol.Interact_186_53
Author(s) : Goncalves JF , Fiorenza AM , Spanevello RM , Mazzanti CM , Bochi GV , Antes FG , Stefanello N , Rubin MA , Dressler VL , Morsch VM , Schetinger MR
Ref : Chemico-Biological Interactions , 186 :53 , 2010
Abstract : The present study investigated the effect of the administration of N-acetylcysteine (NAC), on memory, on acetylcholinesterase (AChE) activity and on lipid peroxidation in different brain structures in cadmium (Cd)-exposed rats. The rats received Cd (2 mg/kg) and NAC (150 mg/kg) by gavage every other day for 30 days. The animals were divided into four groups (n=12-13): control/saline, NAC, Cd, and Cd/NAC. The results showed a decrease in step-down latency in the Cd-group, but NAC reversed the impairment of memory induced by Cd intoxication. Rats exposed to Cd and/or treated with NAC did not demonstrate altered shock sensitivity. Decreased AChE activity was found in hippocampus, cerebellum and hypothalamus in the Cd-group but NAC reversed this effect totally or partially while in cortex synaptosomes and striatum there was no alteration in AChE activity. An increase in TBARS levels was found in hippocampus, cerebellum and hypothalamus in the Cd-group and NAC abolished this effect while in striatum there was no alteration in TBARS levels. Urea and creatinine levels were increased in serum of Cd-intoxicated rats, but NAC was able to abolish these undesirable effects. The present findings show that treatment with NAC prevented the Cd-mediated decrease in AChE activity, as well as oxidative stress and consequent memory impairment in Cd-exposed rats, demonstrating that this compound may modulate cholinergic neurotransmission and consequently improve cognition. However, it is necessary to note that the mild renal failure may be a contributor to the behavioral impairment found in this investigation.
ESTHER : Goncalves_2010_Chem.Biol.Interact_186_53
PubMedSearch : Goncalves_2010_Chem.Biol.Interact_186_53
PubMedID: 20399762

Title : Ectonucleotidase and acetylcholinesterase activities in synaptosomes from the cerebral cortex of streptozotocin-induced diabetic rats and treated with resveratrol - Schmatz_2009_Brain.Res.Bull_80_371
Author(s) : Schmatz R , Mazzanti CM , Spanevello R , Stefanello N , Gutierres J , Maldonado PA , Correa M , da Rosa CS , Becker L , Bagatini M , Goncalves JF , Jaques Jdos S , Schetinger MR , Morsch VM
Ref : Brain Research Bulletin , 80 :371 , 2009
Abstract : The aim of the present study was to investigate the effects of resveratrol (RV), an important neuroprotective compound on NTPDase, 5'-nucleotidase and acetylcholinesterase (AChE) activities in cerebral cortex synaptosomes of streptozotocin (STZ)-induced diabetic rats. The animals were divided into six groups (n=8): control/saline; control/RV 10mg/kg; control/RV 20mg/kg; diabetic/saline; diabetic/RV 10mg/kg; diabetic/RV 20mg/kg. After 30 days of treatment with resveratrol the animals were sacrificed and the cerebral cortex was removed for synaptosomes preparation and enzymatic assays. The results demonstrated that NTPDase and 5'-nucleotidase activities were significantly increased in the diabetic/saline group (p<0.05) compared to control/saline group. Treatment with resveratrol significantly increased NTPDase, 5'-nucleotidase activities in the diabetic/RV10 and diabetic/RV20 groups (p<0.05) compared to diabetic/saline group. When resveratrol was administered per se there was also an increase in the activities of these enzymes in the control/RV10 and control/RV20 groups (p<0.05) compared to control/saline group. AChE activity was significantly increased in the diabetic/saline group (p<0.05) compared to control/saline group. The treatment with resveratrol prevented this increase in the diabetic/RV10 and diabetic/RV20 groups. In conclusion, this study demonstrated that the resveratrol interfere with the purinergic and cholinergic neurotransmission by altering NTPDase, 5'-nucleotidase and AChE activities in cerebral cortex synaptosomes of diabetic rats. In this context, we can suggest that resveratrol should be considered potential therapeutics and scientific tools to be investigated in brain disorders associated with the diabetes.
ESTHER : Schmatz_2009_Brain.Res.Bull_80_371
PubMedSearch : Schmatz_2009_Brain.Res.Bull_80_371
PubMedID: 19723569

Title : Pre-treatment with ebselen and vitamin E modulate acetylcholinesterase activity: interaction with demyelinating agents - Mazzanti_2009_Int.J.Dev.Neurosci_27_73
Author(s) : Mazzanti CM , Spanevello R , Ahmed M , Pereira LB , Goncalves JF , Correa M , Schmatz R , Stefanello N , Leal DB , Mazzanti A , Ramos AT , Martins TB , Danesi CC , Graca DL , Morsch VM , Schetinger MR
Ref : Int J Developmental Neuroscience , 27 :73 , 2009
Abstract : The ethidium bromide (EB) demyelinating model was associated with vitamin E (Vit E) and ebselen (Ebs) treatment to evaluate acetylcholinesterase (AChE) activity in the striatum (ST), hippocampus (HP), cerebral cortex (CC) and erythrocytes. Rats were divided into seven groups: I-Control (saline), II-(canola); III-(Ebs), IV-(Vit E); V-(EB); VI-(EB+Ebs) and VII-(EB+Vit E). At 3 days after the EB injection, AChE activity in the CC and HC was significantly reduced in groups III, IV, V, VI and VII (p<0.05) and in the ST it was reduced in groups III and V (p<0.05) when compared to the control group. At 21 days after the EB injection, AChE activity in the CC was significantly reduced in groups III, IV and V, while in groups VI and VII a significant increase was observed when compared to the control group. In the HC and ST, AChE activity was significantly reduced in groups V, VI and VII when compared to the control group (p<0.05). In the erythrocytes, at 3 days after the EB injection, AChE activity was significantly reduced in groups III, IV, V, VI and VII and at 21 days there was a significant reduction only in groups VI and VII (p<0.05) when compared to the control group. In conclusion, this study demonstrated that Ebs and Vit E interfere with the cholinergic neurotransmission by altering AChE activity in the different brain regions and in the erythrocytes. Furthermore, treatment with Vit E and Ebs protected against the demyelination lesion caused by EB. In this context, we can suggest that ebselen and Vit E should be considered potential therapeutics and scientific tools to be investigated in brain disorders associated with demyelinating events.
ESTHER : Mazzanti_2009_Int.J.Dev.Neurosci_27_73
PubMedSearch : Mazzanti_2009_Int.J.Dev.Neurosci_27_73
PubMedID: 18930802

Title : Effects in vitro of guanidinoacetate on adenine nucleotide hydrolysis and acetylcholinesterase activity in tissues from adult rats - Spanevello_2008_Neurochem.Res_33_1129
Author(s) : Spanevello RM , de Souza Wyse AT , Mazzanti CM , Schmatz R , Stefanello N , Goncalves JF , Bagatini M , Battisti V , Morsch VM , Schetinger MR
Ref : Neurochem Res , 33 :1129 , 2008
Abstract : Guanidinoacetate methyltransferase (GAMT) deficiency is a disorder of creatine metabolism characterized by low plasma creatine concentrations in combination with elevated guanidinoacetate (GAA) concentrations. The aim of this work was to investigate the in vitro effect of guanidinoacetate in NTPDase, 5'-nucleotidase and acetylcholinesterase activities in the synaptosomes, platelets and blood of rats. The results showed that in synaptosomes the NTPDase and 5'-nucleotidase activities were inhibited significantly in the presence of GAA at concentrations of 50, 100, 150 and 200 microM (P < 0.05). However, in platelets GAA at the same concentrations caused a significant increase in the activities of these two enzymes (P < 0.05). In relation to the acetylcholinesterase activity, GAA caused a significant inhibition in the activity of this enzyme in blood at concentrations of 150 and 200 microM (P < 0.05), but did not alter the acetylcholinesterase activity in synaptosomes from the cerebral cortex. Our results suggest that alterations caused by GAA in the activities of these enzymes may contribute to the understanding of the neurological dysfunction of GAMT-deficient patients.
ESTHER : Spanevello_2008_Neurochem.Res_33_1129
PubMedSearch : Spanevello_2008_Neurochem.Res_33_1129
PubMedID: 18256932

Title : Acetylcholinesterase activity in rats experimentally demyelinated with ethidium bromide and treated with interferon beta - Mazzanti_2006_Neurochem.Res_31_1027
Author(s) : Mazzanti CM , Spanevello RM , Pereira LB , Goncalves JF , Kaizer R , Correa M , Ahmed M , Mazzanti A , Festugatto R , Graca DL , Morsch VM , Schetinger MR
Ref : Neurochem Res , 31 :1027 , 2006
Abstract : The ethidium bromide (EB) demyelinating model was associated with interferon beta (IFN-beta) to evaluate acetylcholinesterase (AChE) activity in the striatum (ST), hippocampus (HP), cerebral cortex (CC), cerebellum (CB), hypothalamus (HY), pons (PN) and synaptosomes from the CC. Rats were divided into four groups: I control (saline), II (IFN-beta), III (EB) and IV (EB and IFN-beta). After 7, 15 and 30 days rats (n = 6) were sacrificed, and the brain structures were removed for enzymatic assay. AChE activity was found to vary in all the brain structures in accordance with the day studied (7-15-30 days) (P < 0.05). In the group III, there was an inhibition of the AChE activity in the ST, CB, HY, HP and also in synaptosomes of the CC (P < 0.05). It was observed that IFN-beta per se was capable to significantly inhibit (P < 0.05) AChE activity in the ST, HP, HY and synaptosomes of the CC. Our results suggest that one of the mechanisms of action of IFN-beta is through the inhibition of AChE activity, and EB could be considered an inhibitor of AChE activity by interfering with cholinergic neurotransmission in the different brain regions.
ESTHER : Mazzanti_2006_Neurochem.Res_31_1027
PubMedSearch : Mazzanti_2006_Neurochem.Res_31_1027
PubMedID: 16871442

Title : Serum cholinesterase activity in diabetes and associated pathologies - Inacio_2006_Diabetes.Res.Clin.Pract_72_28
Author(s) : Inacio Lunkes G , Stefanello F , Sausen Lunkes D , Maria Morsch V , Schetinger MR , Goncalves JF
Ref : Diabetes Res Clin Pract , 72 :28 , 2006
Abstract : Serum cholinesterase activity was measured in diabetes, hypertensive and diabetic/hypertensive patients. The sample consisted of volunteer patients and was divided in a control group (n=26), type 2 diabetic group (n=16), hypertensive group (n=12) and type 2 diabetic/hypertensive group (n=26). In addition, blood glucose, cholesterol and triglyceride levels were determined. Serum cholinesterase activity in the control group was significantly lower in relation to the other groups (p<0.001). Blood glucose levels were elevated in type 2 diabetic and type 2 diabetic/hypertensive groups. In vitro studies showed increased cholinesterase activity in the presence of glucose 5-100mM or insulin 0.5-25 UI (p<0.001). Cholesterol and triglycerides were at normal levels only in the control group. Possibly, a relationship exists between the increase in serum cholinesterase and the vascular complications in the diabetic patients, potentially stimulated by the levels of glycemia and dyslipidemia. Although patients were receiving different medicines, the increase in enzyme activity was similar in all groups. This enzymatic profile suggests a possible interference of the diseases in the catalytic mechanism of the serum cholinesterase enzyme.
ESTHER : Inacio_2006_Diabetes.Res.Clin.Pract_72_28
PubMedSearch : Inacio_2006_Diabetes.Res.Clin.Pract_72_28
PubMedID: 16233931

Title : Acetylcholinesterase activation and enhanced lipid peroxidation after long-term exposure to low levels of aluminum on different mouse brain regions - Kaizer_2005_J.Inorg.Biochem_99_1865
Author(s) : Kaizer RR , Correa MC , Spanevello RM , Morsch VM , Mazzanti CM , Goncalves JF , Schetinger MR
Ref : J Inorg Biochem , 99 :1865 , 2005
Abstract : Aluminum (Al), oxidative stress and impaired cholinergic functions have all been related to Alzheimer's disease (AD). The present study evaluates the effect of aluminum on acetylcholinesterase (AChE) and lipid peroxidation in the mouse brain. Mice were loaded by gavage with Al 0.1 mmol/kg/day 5 days per week during 12 weeks. The mice were divided into four groups: (1) control; (2) 10 mg/mL of citrate solution; (3) 0.1 mmol/kg of Al solution; (4) 0.1 mmol/kg of Al plus 10 mg/mL of citrate solution. AChE activity was determined in the hippocampus, striatum, cortex, hypothalamus and cerebellum and lipid peroxidation was determined in the hippocampus, striatum and cortex. An increase of AChE activity was observed in the fourth group (Al + Ci) in the hippocampus (36%), striatum (54%), cortex (44%) and hypothalamus (22%) (p<0.01). The third group (Al) presented a decrease of AChE activity in the hypothalamus (20%) and an enhancement in the striatum (27%). Lipid peroxidation, measured by TBARS (thiobarbituric acid reactive substances), was elevated in the hippocampus and cerebral cortex when compared with the control (p < 0.01). The effect of aluminum on AChE activity may be due to a direct neurotoxic effect of the metal or perhaps a disarrangement of the plasmatic membrane caused by increased lipid peroxidation.
ESTHER : Kaizer_2005_J.Inorg.Biochem_99_1865
PubMedSearch : Kaizer_2005_J.Inorg.Biochem_99_1865
PubMedID: 16055195