Mazzanti CM

References (30)

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 : Anthocyanins restore behavioral and biochemical changes caused by streptozotocin-induced sporadic dementia of Alzheimer's type - Gutierres_2014_Life.Sci_96_7
Author(s) : Gutierres JM , Carvalho FB , Schetinger MR , Marisco P , Agostinho P , Rodrigues M , Rubin MA , Schmatz R , da Silva CR , de PCG , Farias JG , Signor C , Morsch VM , Mazzanti CM , Bogo M , Bonan CD , Spanevello R
Ref : Life Sciences , 96 :7 , 2014
Abstract : AIMS: The aim of this study was to analyze if the pre-administration of anthocyanin on memory and anxiety prevented the effects caused by intracerebroventricular streptozotocin (icv-STZ) administration-induced sporadic dementia of Alzheimer's type (SDAT) in rats. Moreover, we evaluated whether the levels of nitrite/nitrate (NOx), Na(+),K(+)-ATPase, Ca(2+)-ATPase and acethylcholinesterase (AChE) activities in the cerebral cortex (CC) and hippocampus (HC) are altered in this experimental SDAT. MAIN
METHODS: Male Wistar rats were divided in 4 different groups: control (CTRL), anthocyanin (ANT), streptozotocin (STZ) and streptozotocin+anthocyanin (STZ+ANT). After seven days of treatment with ANT (200mg/kg; oral), the rats were icv-STZ injected (3mg/kg), and four days later the behavior parameters were performed and the animals submitted to euthanasia. KEY FINDINGS: A memory deficit was found in the STZ group, but ANT treatment showed that it prevents this impairment of memory (P<0.05). Our results showed a higher anxiety in the icv-STZ group, but treatment with ANT showed a per se effect and prevented the anxiogenic behavior induced by STZ. Our results reveal that the ANT treatment (100muM) tested displaces the specific binding of [(3)H] flunitrazepam to the benzodiazepinic site of GABAA receptors. AChE, Ca(+)-ATPase activities and NOx levels were found to be increased in HC and CC in the STZ group, which was attenuated by ANT (P<0.05). STZ decreased Na(+),K(+)-ATPase activity and ANT was able to prevent these effects (P<0.05). SIGNIFICANCE: In conclusion, these findings demonstrated that ANT is able to regulate ion pump activity and cholinergic neurotransmission, as well as being able to enhance memory and act as an anxiolytic compound in animals with SDAT.
ESTHER : Gutierres_2014_Life.Sci_96_7
PubMedSearch : Gutierres_2014_Life.Sci_96_7
PubMedID: 24291256

Title : Neuroprotective role of quercetin in locomotor activities and cholinergic neurotransmission in rats experimentally demyelinated with ethidium bromide - Beckmann_2014_Life.Sci_103_79
Author(s) : Beckmann DV , Carvalho FB , Mazzanti CM , Dos Santos RP , Andrades AO , Aiello G , Rippilinger A , Graca DL , Abdalla FH , Oliveira LS , Gutierres JM , Schetinger MR , Mazzanti A
Ref : Life Sciences , 103 :79 , 2014
Abstract : AIM: The purpose of this study was to investigate whether the flavonoid quercetin can prevent alterations in the behavioral tests and of cholinergic neurotransmission in rats submitted to the ethidium bromide (EB) experimental demyelination model during events of demyelination and remyelination. MAIN
METHODS: Wistar rats were randomly distributed into four groups (20 animals per group): Control (pontine saline injection and treatment with ethanol), Querc (pontine saline injection and treatment with quercetin), EB (pontine 0.1% EB injection and treatment with ethanol), and EB+Querc (pontine 0.1% EB injection and treatment with quercetin). The groups Querc and Querc+EB were treated once daily with quercetin (50mg/kg) diluted in 25% ethanol solution (1ml/kg) and the animals of the control and EB groups were treated once daily with 25% ethanol solution (1ml/kg). Two stages were observed: phase of demyelination (peak on day 7) and phase of remyelination (peak on day 21 post-injection). Behavioral tests (beam walking, foot fault and inclined plane test), acetylcholinesterase (AChE) activity and lipid peroxidation in pons, cerebellum, hippocampus, hypothalamus, striatum and cerebral cortex were measured. KEY FINDINGS: The quercetin promoted earlier locomotor recovery, suggesting that there was demyelination prevention or further remyelination velocity as well as it was able to prevent the inhibition of AChE activity and the increase of lipidic peroxidation, suggesting that this compound can protect cholinergic neurotransmission. SIGNIFICANCE: These results may contribute to a better understanding of the neuroprotective role of quercetin and the importance of an antioxidant diet in humans to provide benefits in neurodegenerative diseases such as MS.
ESTHER : Beckmann_2014_Life.Sci_103_79
PubMedSearch : Beckmann_2014_Life.Sci_103_79
PubMedID: 24727240

Title : Effects of chlorogenic acid, caffeine, and coffee on behavioral and biochemical parameters of diabetic rats - Stefanello_2014_Mol.Cell.Biochem_388_277
Author(s) : Stefanello N , Schmatz R , Pereira LB , Rubin MA , da Rocha JB , Facco G , Pereira ME , Mazzanti CM , Passamonti S , Rodrigues MV , Carvalho FB , da Rosa MM , Gutierres JM , Cardoso AM , Morsch VM , Schetinger MR
Ref : Molecular & Cellular Biochemistry , 388 :277 , 2014
Abstract : Diabetes mellitus (DM) is associated with brain alterations that may contribute to cognitive dysfunctions. Chlorogenic acid (CGA) and caffeine (CA), abundant in coffee (CF), are natural compounds that have showed important actions in the brain. The present study aimed to evaluate the effect of CGA, CA, and CF on acetylcholinesterase (AChE), Na(+), K(+)-ATPase, aminolevulinate dehydratase (delta-ALA-D) activities and TBARS levels from cerebral cortex, as well as memory and anxiety in streptozotocin-induced diabetic rats. Animals were divided into eight groups (n = 5-10): control; control/CGA 5 mg/kg; control/CA 15 mg/kg; control/CF 0.5 g/kg; diabetic; diabetic/CGA 5 mg/kg; diabetic/CA 15 mg/kg; and diabetic/CF 0.5 g/kg. Our results demonstrated an increase in AChE activity and TBARS levels in cerebral cortex, while delta-ALA-D and Na(+), K(+)-ATPase activities were decreased in the diabetic rats when compared to control water group. Furthermore, a memory deficit and an increase in anxiety in diabetic rats were observed. The treatment with CGA and CA prevented the increase in AChE activity in diabetic rats when compared to the diabetic water group. CGA, CA, and CF intake partially prevented cerebral delta-ALA-D and Na(+), K(+)-ATPase activity decrease due to diabetes. Moreover, CGA prevented diabetes-induced TBARS production, improved memory, and decreased anxiety. In conclusion, among the compounds studied CGA proved to be a compound which acts better in the prevention of brain disorders promoted by DM.
ESTHER : Stefanello_2014_Mol.Cell.Biochem_388_277
PubMedSearch : Stefanello_2014_Mol.Cell.Biochem_388_277
PubMedID: 24370728

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 : Neuroprotective effect of anthocyanins on acetylcholinesterase activity and attenuation of scopolamine-induced amnesia in rats - Gutierres_2013_Int.J.Dev.Neurosci_33C_88
Author(s) : Gutierres JM , Carvalho FB , Schetinger MR , Agostinho P , Marisco PC , Vieira JM , Rosa MM , Bohnert C , Rubin MA , Morsch VM , Spanevello R , Mazzanti CM
Ref : Int J Developmental Neuroscience , 33C :88 , 2013
Abstract : Anthocyanins are a group of natural phenolic compounds responsible for the color to plants and fruits. These compounds might have beneficial effects on memory and have antioxidant properties. In the present study we have investigated the therapeutic efficacy of anthocyanins in an animal model of cognitive deficits, associated to Alzheimer's disease, induced by scopolamine. We evaluated whether anthocyanins protect the effects caused by SCO on nitrite/nitrate (NOx) levels and Na+,K+-ATPase and Ca2+-ATPase and acetylcholinesterase (AChE) activities in the cerebral cortex and hippocampus (of rats. We used 4 different groups of animals: control (CTRL), anthocyanins treated (ANT), scopolamine-challenged (SCO), and scopolamine+anthocyanins (SCO+ANT). After seven days of treatment with ANT (200mgkg-1; oral), the animals were SCO injected (1mgkg-1; IP) and were performed the behavior tests, and submitted to euthanasia. A memory deficit was found in SCO group, but ANT treatment prevented this impairment of memory (P<0.05). The ANT treatment per se had an anxiolytic effect. AChE activity was increased in both in cortex and hippocampus of SCO group, this effect was significantly attenuated by ANT (P<0.05). SCO decreased Na+,K+-ATPase and Ca2+-ATPase activities in hippocampus, and ANT was able to significantly (P<0.05) prevent these effects. No significant alteration was found on NOx levels among the groups. In conclusion, the ANT is able to regulate cholinergic neurotransmission and restore the Na+,K+-ATPase and Ca2+-ATPase activities, and also prevented memory deficits caused by scopolamine administration.
ESTHER : Gutierres_2013_Int.J.Dev.Neurosci_33C_88
PubMedSearch : Gutierres_2013_Int.J.Dev.Neurosci_33C_88
PubMedID: 24374256

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 : Biochemistry detection of acetylcholinesterase activity in Trypanosoma evansi and possible functional correlations - Wolkmer_2012_Exp.Parasitol_132_546
Author(s) : Wolkmer P , da Silva CB , Paim FC , Da Silva AS , Tavares KC , Lazzarotto CR , Palma HE , Thome GR , Miletti LC , Schetinger MR , Lopes ST , Mazzanti CM
Ref : Experimental Parasitology , 132 :546 , 2012
Abstract : Several chemical and immunohistochemical techniques can be used for the detection of acetylcholinesterase (AChE) activity. In this experiment we aimed to detect AChE activity in Trypanosoma evansi. For this, the parasites were isolated from the blood of experimentally infected rats using a DEA-cellulose column. Enzymatic activity was determined in trypomastigote forms at 0, 0.2, 0.4, 0.8 and 1.2mg/mL of protein concentrations by a standard biochemical protocol. At all concentrations tested, the study showed that T. evansi expresses the enzyme AChE and its activity was proportional to the concentration of protein, ranging between 0.64 and 2.70mumol of AcSCh/h. Therefore, we concluded that it is possible to biochemically detect AChE in T. evansi, an enzyme that may be associated with vital functions of the parasite and also can be related to chemotherapy treatments, as further discussed in this article.
ESTHER : Wolkmer_2012_Exp.Parasitol_132_546
PubMedSearch : Wolkmer_2012_Exp.Parasitol_132_546
PubMedID: 22981718

Title : 17-beta estradiol in the acetylcholinesterase activity and lipid peroxidation in the brain and blood of ovariectomized adult and middle-aged rats - Martins_2012_Life.Sci_90_351
Author(s) : Martins DB , Mazzanti CM , Franca RT , Pagnoncelli M , Costa MM , de Souza EM , Goncalves J , Spanevello R , Schmatz R , da Costa P , Mazzanti A , Beckmann DV , Cecim Mda S , Schetinger MR , Lopes ST
Ref : Life Sciences , 90 :351 , 2012
Abstract : AIMS: To investigate the 17-beta estradiol in the acetylcholinesterase activity and lipid peroxidation in the brain and blood of ovariectomized rats of different ages. MAIN METHODS: Animals were randomly assigned into three experimental groups of each age (n=6). Control groups consisted of adult (sham-A) and middle-aged (sham-MA) female rats, ovariectomized adult (OVX-A) and middle-aged (OVX-MA) rats without estrogen therapy reposition, and ovariectomized adult (OVX+E2-A) and middle-aged (OVX+E2-MA) rats treated with 17-beta estradiol for 30days. After this period, AChE activity and lipid peroxidation were measured in the brain and blood. KEY FINDINGS: The AChE activity increased (p<0.05) in striatum (ST) in OVX-A, OVX+E2-A and OVX-MA, and hippocampus (HP) in OVX-MA. The enzyme activity decreased (p<0.05) in ST of OVX+E2-MA, and cerebral cortex (CC) in OVX+E2-A, OVX-MA and OVX+E2-MA. Blood AChE activity increased (p<0.05) in OVX+E2-A and decreased (p<0.05) in OVX-MA. Lymphocyte AChE activity increased (p<0.05) in OVX-A and OVX+E2-A and decreased (p<0.05) in OVX-MA. Lipid peroxidation increased (p<0.05) in ST of OVX-A, CC of OVX-A and OVX-MA, HP of OVX-A, and cerebellum (CE) of OVX-A, OVX-MA, and OVX+E2-MA. Lipid peroxidation decreased (p<0.05) in ST, CC and CE of OVX+E2-A, and ST and HP of OVX+E2-MA. Similar values of lipid peroxidation to control groups were found in ST and HP of OVX-MA, HP of OVX+E2-A and CC of OVX+E2-MA. SIGNIFICANCE: 17-beta estradiol is able to modulate the AChE activity and non-neuronal cholinergic response as well as to reduce lipid peroxidation. Its response is dependent on the age and brain structure analyzed.
ESTHER : Martins_2012_Life.Sci_90_351
PubMedSearch : Martins_2012_Life.Sci_90_351
PubMedID: 22227472

Title : Diphenyl diselenide ameliorates cognitive deficits induced by a model of menopause in rats - da Rocha_2012_Behav.Pharmacol_23_98
Author(s) : da Rocha JT , Pinton S , Mazzanti A , Mazzanti CM , Beckemann DV , Nogueira CW , Zeni G
Ref : Behav Pharmacol , 23 :98 , 2012
Abstract : Ovarian hormone loss contributes to cognitive decline in postmenopausal women. Studies have demonstrated a positive role of the level of the element selenium in cognitive performance. The present study investigated the effects of the synthetic organoselenium compound diphenyl diselenide (PhSe)(2) on cognitive functions in ovariectomized rats. Ninety-day-old female Wistar rats were subjected to ovariectomy (OVX) or Sham operation. One week after surgery, rats were orally treated with (PhSe)(2) (5 mg/kg, per oral route) or vehicle once a day for 30 days. Next, the rats were evaluated in behavioral tests [Morris water maze (MWM) and open-field tests] and biochemical [cerebral acetylcholinesterase (AChE)] analyses were carried out. In MWM probe trial, (PhSe)(2) decreased the latency to reach the platform location and increased the number of crossings over the platform location, protecting against cognitive impairment induced by OVX. Furthermore, (PhSe)(2) prevented the stimulation of AChE activity caused by OVX. In conclusion, the present study showed a cognition-enhancing effect of (PhSe)(2) treatment for 30 days in ovariectomized rats in the MWM test, which could be related to its ability to prevent the stimulation of AChE activity caused by OVX in rats. These findings suggest that (PhSe)(2) might have a promising role in preventing the cognitive decline related to menopause.
ESTHER : da Rocha_2012_Behav.Pharmacol_23_98
PubMedSearch : da Rocha_2012_Behav.Pharmacol_23_98
PubMedID: 22139607

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 : Pre-treatment with curcumin modulates acetylcholinesterase activity and proinflammatory cytokines in rats infected with Trypanosoma evansi - Wolkmer_2012_Parasitol.Int_62_144
Author(s) : Wolkmer P , da Silva CB , Paim FC , Duarte MM , Castro V , Palma HE , Franca RT , Felin DV , Siqueira LC , Lopes ST , Schetinger MR , Monteiro SG , Mazzanti CM
Ref : Parasitol Int , 62 :144 , 2012
Abstract : The potent activity against Trypanosomes and health beneficial effects of curcumin (Cur) has been demonstrated in various experimental models. In this study, we evaluated the in vivo effect of Cur as trypanocide and as potential anti-inflammatory agent, through the evaluation of immunomodulatory mechanisms in rats infected with Trypanosoma evansi. Daily oral Cur was administered at doses of 0, 20 or 60mg/kg as preventive treatment (30 and 15days pre infection) and as treatment (post infection). The treatment of the groups continued until the day of euthanasia. Fifteen days after inoculation, parasitemia, plasma proinflammatory cytokines (IFN-gamma, TNF-alpha, IL-1, IL-6), anti-inflammatory cytokines (IL-10) and blood acetylcholinesterase activity (AChE) were analyzed. Pretreatment with Cur reduced parasitemia and lethality. Cur inhibited AChE activity and improved immunological response by cytokines proinflammatory, fundamental during T. evansi infection. We found that Cur is not so important as an antitrypanosomal activity but as immunomodulator agent. These findings reveal that the preventive use of Cur stimulates anti-inflammatory mechanisms, reducing an excessive inflammatory response.
ESTHER : Wolkmer_2012_Parasitol.Int_62_144
PubMedSearch : Wolkmer_2012_Parasitol.Int_62_144
PubMedID: 23200738

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 : Vitamin E decreased the activity of acetylcholinesterase and level of lipid peroxidation in brain of rats exposed to aged and diluted sidestream smoke - Thome_2011_Nicotine.Tob.Res_13_1210
Author(s) : Thome GR , Spanevello RM , Mazzanti A , Fiorenza AM , Duarte MM , da Luz SC , Pereira ME , Morsch VM , Schetinger MR , Mazzanti CM
Ref : Nicotine Tob Res , 13 :1210 , 2011
Abstract : INTRODUCTION: The biological systems of both smoker and passive smoking suffer changes caused by toxic compounds from cigarette smoke such as inflammation, lipid peroxidation, and deficiency of vitamin E. The aim of the present study was to evaluate the effect of vitamin E on acetylcholinesterase (AChE) activity and the lipid peroxidation level in the brain of rats in the model of exposure to aged and diluted sidestream smoke (ADSS). METHODS: Adult male Wistar rats (200-300 g) were exposed to ADSS for 4 weeks and treated with vitamin E (50 mg/kg/day) loaded by gavage. In the first, second, third, and fourth weeks, animals were concomitantly exposed to the smoke of 1, 2, 3, and 4 cigarettes/day, respectively. The duration of each exposure was 15 min, daily. RESULTS: For rats exposed to ADSS, the AChE activity and lipid peroxidation level increased in the striatum, cerebral cortex, and cerebellum. In contrast, the activity of AChE and the level of lipid peroxidation decreased in the smoke group treated with vitamin E. CONCLUSIONS: The results suggest that the rats exposed to ADSS and treated with vitamin E significantly reduced the raised activity of AChE and level lipid peroxidation from the brain structures studied. The study, therefore, concludes that vitamin E could be considered as a therapeutic agent in this type of exposure.
ESTHER : Thome_2011_Nicotine.Tob.Res_13_1210
PubMedSearch : Thome_2011_Nicotine.Tob.Res_13_1210
PubMedID: 21896885

Title : Trypanosoma evansi: cholinesterase activity in acutely infected Wistar rats - Wolkmer_2010_Exp.Parasitol_125_251
Author(s) : Wolkmer P , Lopes ST , Franciscato C , Da Silva AS , Traesel CK , Siqueira LC , Pereira ME , Monteiro SG , Mazzanti CM
Ref : Experimental Parasitology , 125 :251 , 2010
Abstract : The aim of this study was to evaluate cholinesterase activity during the early acute phase of Trypanosoma evansi infection in rats. Fifteen male Wistar rats were randomly distributed into three groups (n=5 animals per group): two trypanosome-infected groups (T3 and T5) and uninfected controls (C). The animals were inoculated intraperitoneally with 10(6) trypanosomes. The blood was collected by cardiac puncture on the 3rd (T3) or 5th day post-infection (T5 and C). Cerebrum and cerebellum were removed for the evaluation of acetylcholinesterase (AChE) activity. AChE activity was also evaluated in whole blood and butyrylcholinesterase activity (BUChE) in plasma samples. Parasitemia were progressive increase and parasites were observed in the peripheral blood of all infected animals one day post-inoculation. AChE activity was not altered in cerebrum and cerebellum tissues. AChE activity in blood significantly decreased in the T3 and T5 groups (26.63 and 25.86mU/lmolHb) compared with the control (37.84mU/lmolHb). In addition BUChE activity in plasma was lower in the T3 (7.01micromol BTC hydrolyzed/h/mL) than the T5 and C groups (9.84 and 12.00micromol BTC hydrolyzed/h/mL). This study therefore, shows that reductions in the activity of cholinesterase occur in acute infection by T. evansi in rats and this demonstrates an important change occurring in animals infected by the protozoan and may indicate a potential role the enzymes play in the mechanism of disease.
ESTHER : Wolkmer_2010_Exp.Parasitol_125_251
PubMedSearch : Wolkmer_2010_Exp.Parasitol_125_251
PubMedID: 20138875

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 : Resveratrol prevents memory deficits and the increase in acetylcholinesterase activity in streptozotocin-induced diabetic rats - Schmatz_2009_Eur.J.Pharmacol_610_42
Author(s) : Schmatz R , Mazzanti CM , Spanevello R , Stefanello N , Gutierres J , Correa M , da Rosa MM , Rubin MA , Chitolina Schetinger MR , Morsch VM
Ref : European Journal of Pharmacology , 610 :42 , 2009
Abstract : The objective of the present study was to investigate the effect of the administration of resveratrol (RV) on memory and on acetylcholinesterase (AChE) activity in the cerebral cortex, hippocampus, striatum, hypothalamus, cerebellum and blood in streptozotocin-induced diabetic rats. The animals were divided into six groups (n=6-13): Control/saline; Control/RV 10 mg/kg; Control/RV 20 mg/kg; Diabetic/saline; Diabetic/RV 10 mg/kg; Diabetic/RV 20 mg/kg. One day after 30 days of treatment with resveratrol the animals were submitted to behavioral tests and then submitted to euthanasia and the brain structures and blood were collected. The results showed a decrease in step-down latency in diabetic/saline group. Resveratrol (10 and 20 mg/kg) prevented the impairment of memory induced by diabetes. In the open field test, no significant differences were observed between the groups. In relation to AChE activity, a significant increase in diabetic/saline group (P<0.05) was observed in all brain structures compared to control/saline group. However, AChE activity decreased significantly in control/RV10 and control/RV20 (P<0.05) groups in cerebral cortex, hippocampus and striatum, while no significant differences were observed in diabetic/RV10 and diabetic/RV20 groups in all brain structures compared to control/saline group. Blood AChE activity increased significantly in diabetic/saline group (P<0.05) decreased in control/RV10, control/RV20 and diabetic/RV20 groups (P<0.05) compared to control/saline group. In conclusion, the present findings showed that treatment with resveratrol prevents the increase in AChE activity and consequently memory impairment in diabetic rats, demonstrating that this compound can modulate cholinergic neurotransmission and consequently improve cognition.
ESTHER : Schmatz_2009_Eur.J.Pharmacol_610_42
PubMedSearch : Schmatz_2009_Eur.J.Pharmacol_610_42
PubMedID: 19303406

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 : Comparative study of the inhibitory effect of antidepressants on cholinesterase activity in Bungarus sindanus (krait) venom, human serum and rat striatum - Ahmed_2008_J.Enzyme.Inhib.Med.Chem_23_912
Author(s) : Ahmed M , Batista J , Rocha T , Mazzanti CM , Hassan W , Morsch VM , Loro VL , Thome G , Schetinger MR
Ref : J Enzyme Inhib Med Chem , 23 :912 , 2008
Abstract : Cholinesterases are divided into two classes based on differences in their substrate specificity and tissue distribution: acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). These enzymes may be inhibited by several compounds, such as antidepressants. The antidepressants paroxetine, imipramine, clomipramine and sertraline inhibited both venom AChE as well as human serum BChE in a concentration-dependent manner but had no effect on AChE in the rat brain striatum. The IC(50) of venom calculated for imipramine was 0.3 mM, paroxetine 0.38 mM, clomipramine 0.34 mM and sertraline 0.35 mM. Analysis of kinetic data indicated that the inhibition caused by sertraline and paroxetine was mixed, i.e. K(m) values increased and V(max) decreased in a concentration dependent manner. Imipramine and clomipramine exhibited competitive inhibition, i.e. K(m) values increased and V(max) remained constant. The present results suggest that these therapeutic agents used for depression can also be considered as inhibitors of snake venom and human serum cholinesterase.
ESTHER : Ahmed_2008_J.Enzyme.Inhib.Med.Chem_23_912
PubMedSearch : Ahmed_2008_J.Enzyme.Inhib.Med.Chem_23_912
PubMedID: 18608756

Title : Malathion, carbofuran and paraquat inhibit Bungarus sindanus (krait) venom acetylcholinesterase and human serum butyrylcholinesterase in vitro - Ahmed_2007_Ecotoxicology_16_363
Author(s) : Ahmed M , Rocha JB , Mazzanti CM , Morsch AL , Cargnelutti D , Correa M , Loro V , Morsch VM , Schetinger MR
Ref : Ecotoxicology , 16 :363 , 2007
Abstract : Carbofuran and malathion, well known pesticides, and paraquat, a world widely used herbicide, were tested on acetylcholinesterase (AChE) from Bungarus sindanus venom and butyrylcholinesterase (BChE) from human serum. The calculated IC(50 )values for inhibition of venom enzyme by malathion, carbofuran and paraquat were 2.5, 0.14, and 0.16 microM, respectively. The values for inhibition of serum butyrylcholinesterase (BChE) were 3.5, 0.09 and 0.18 microM, respectively. Analysis of kinetic data indicated that the inhibition caused by malathion, carbofuran and paraquat was mixed for venom AChE. For BChE from human serum, the inhibition caused by malathion and paraquat was mixed and for carbofuran it was uncompetitive. The present results suggest a commercial paraquat preparation (a popular herbicide) inhibits cholinesterases with similar or higher potency than classical pesticide inhibitors. Furthermore, this inhibition was observed both in human serum and snake venom, a newly studied source of AChE.
ESTHER : Ahmed_2007_Ecotoxicology_16_363
PubMedSearch : Ahmed_2007_Ecotoxicology_16_363
PubMedID: 17364237

Title : Cyclosporine A inhibits acetylcholinesterase activity in rats experimentally demyelinated with ethidium bromide - Mazzanti_2007_Int.J.Dev.Neurosci_25_259
Author(s) : Mazzanti CM , Spanevello R , Ahmed M , Schmatz R , Mazzanti A , Salbego FZ , Graca DL , Sallis ES , Morsch VM , Schetinger MR
Ref : Int J Developmental Neuroscience , 25 :259 , 2007
Abstract : Cyclosporine A is the major immunosuppressive agent used for organ transplantation and for the treatment of a variety of autoimmune disorders such as multiple sclerosis. In this work, we investigated the effect of the cyclosporine A on the acetylcholinesterase activity in the cerebral cortex, striatum, hippocampus, hypothalamus, cerebellum and pons of the rats experimentally demyelinated by ethidium bromide. Rats were divided into four groups: I control (injected with saline), II (treated with cyclosporine A), III (injected with 0.1% ethidium bromide) and IV (injected with 0.1% the ethidium bromide and treated with cyclosporine A). The results showed a significant inhibition (p<0.05) of acetylcholinesterase activity in the groups II, III and IV in all brain structures analyzed. In the striatum, hippocampus, hypothalamus and pons the inhibition was greater (p<0.005) when ethidium bromide was associated with cyclosporine A. In conclusion, the present investigation demonstrated that cyclosporine A is an inhibitor of acetylcholinesterase activity and this effect is increased after an event of toxic demyelination of the central nervous system.
ESTHER : Mazzanti_2007_Int.J.Dev.Neurosci_25_259
PubMedSearch : Mazzanti_2007_Int.J.Dev.Neurosci_25_259
PubMedID: 17467222

Title : Inhibition of two different cholinesterases by tacrine - Ahmed_2006_Chem.Biol.Interact_162_165
Author(s) : Ahmed M , Rocha JB , Correa M , Mazzanti CM , Zanin RF , Morsch AL , Morsch VM , Schetinger MR
Ref : Chemico-Biological Interactions , 162 :165 , 2006
Abstract : Kinetic parameters of the effect of tacrine as a cholinesterase inhibitor have been studied in two different sources: snake venom (Bungarus sindanus) acetylcholinesterase (AChE) and human serum butyrylcholinesterase (BChE). Tacrine inhibited both venom acetylcholinesterase (AChE) as well as human serum butyrylcholinesterase (BChE) in a concentration-dependent manner. Kinetic studies indicated that the nature of inhibition was mixed for both enzymes, i.e. Km values increase and Vmax decrease with the increase of the tacrine concentration. The calculated IC50 for snake venom and for human serum were 31 and 25.6 nM, respectively. Ki was observed to be 13 nM for venom acetylcholinesterase (AChE) and 12 nM for serum butyrylcholinesterase (BChE). KI (constant of AChE-ASCh-tacrine complex into AChE-ASCh complex and tacrine) was estimated to be 20 nM for venom and 10 nM for serum butyrylcholinesterase (BChE), while the gammaKm (dissociation constant of AChE-ASCh-tacrine complex into AChE-tacrine complex and ASCh) were 0.086 and 0.147 mM for snake venom AChE and serum BChE, respectively. The present results suggest that this therapeutic agent used for the treatment of Alzheimer's disease can also be considered an inhibitor of snake venom and human serum butyrylcholinesterase. Values of Ki and KI show that tacrine had more affinity with these enzymes as compared with other cholinesterases from the literature.
ESTHER : Ahmed_2006_Chem.Biol.Interact_162_165
PubMedSearch : Ahmed_2006_Chem.Biol.Interact_162_165
PubMedID: 16860785

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 : Ethidium bromide inhibits rat brain acetylcholinesterase activity in vitro - Mazzanti_2006_Chem.Biol.Interact_162_121
Author(s) : Mazzanti CM , Spanevello RM , Obregon A , Pereira LB , Streher CA , Ahmed M , Mazzanti A , Graca DL , Morsch VM , Schetinger MR
Ref : Chemico-Biological Interactions , 162 :121 , 2006
Abstract : Ethidium bromide (EtBr), a fluorescent dark red compound and stain for double-stranded DNA and RNA was used to study acetylcholinesterase (AChE) activity in vitro together with kinetic parameters of this enzyme in the striatum (ST), hippocampus (HP), cerebral cortex (CC) and cerebellum (CB) of adult rats. AChE activity in vitro in the ST, HP, CC and CB was significantly reduced (p<0.05) in the presence of EtBr at concentrations of 0.00625, 0.0125, 0.025, 0.05 and 0.1 mM. For the analysis of the kinetic three concentrations of EtBr were tested (0.00625, 0.025 and 0.1 mM). An uncompetitive inhibition type was observed in the ST, HP and CC, whereas in the CB the inhibition type was mixed. These data indicate that EtBr should be considered a strong inhibitor of AChE activity demonstrating that there is an interaction between this compound and the cholinergic system.
ESTHER : Mazzanti_2006_Chem.Biol.Interact_162_121
PubMedSearch : Mazzanti_2006_Chem.Biol.Interact_162_121
PubMedID: 16839531

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