Spanevello R

References (15)

Title : Therapeutic potential of blackberry extract in the preventing memory deficits and neurochemical alterations in the cerebral cortex, hippocampus and cerebellum of a rat model with amnesia - de Mello_2023_Metab.Brain.Dis__
Author(s) : de Mello JE , Luduvico KP , Dos Santos A , Teixeira FC , de Souza Cardoso J , de Aguiar MSS , Cunico W , Vizzotto M , Stefanello F , Spanevello R
Ref : Metabolic Brain Disease , : , 2023
Abstract : The blackberry (Rubus sp.) is a popular fruit that has a high concentration of phenolic compounds. Pharmacological investigations have demonstrated the important biological activities of the blackberry extract, such as neuroprotective actions. This study aimed to evaluate the effects of blackberry extract on memory and neurochemical parameters in rats subjected to scopolamine (SCO)-induced amnesia. Male rats were divided into five groups: I, control (saline); II, SCO; III, SCO + Rubus sp. (100 mg/kg); IV, SCO + Rubus sp. (200 mg/kg); and V, SCO + donepezil (5 mg/kg). Blackberry extract and donepezil were orally administered for 10 days. On day 11, group I received saline, and groups II, III, IV, and V received SCO (1 mg/kg) intraperitoneally after object recognition behavioral training. Twenty-four hours after the training session, animals were subjected to an object recognition test. Finally, the animals were euthanized, and the cerebral cortex, hippocampus, and cerebellum were collected to evaluate the oxidative stress and acetylcholinesterase (AChE) activity. Rubus sp. extract prevented memory impairment induced by SCO in a manner similar to that of donepezil. Additionally, Rubus sp. extract and donepezil prevented the increase in AChE activity induced by SCO in all the evaluated brain structures. SCO induced oxidative damage in the cerebral cortex, hippocampus, and cerebellum, which was prevented by Rubus sp. and donepezil. Our results suggest that the antioxidant and anticholinesterase activities of Rubus sp. are associated with memory improvement; hence, it can potentially be used for the treatment of neurodegenerative diseases.
ESTHER : de Mello_2023_Metab.Brain.Dis__
PubMedSearch : de Mello_2023_Metab.Brain.Dis__
PubMedID: 36735154

Title : Gallic acid protects cerebral cortex, hippocampus, and striatum against oxidative damage and cholinergic dysfunction in an experimental model of manic-like behavior: comparison with lithium effects - Recart_2021_Int.J.Dev.Neurosci__
Author(s) : Recart VM , Spohr L , Soares MSP , da Silveira de Mattos B , Bona NP , Pedra NS , Teixeira FC , Gamaro GD , Stefanello F , Spanevello R
Ref : Int J Developmental Neuroscience , : , 2021
Abstract : Bipolar disorder is characterized by episodes of depression and mania, and oxidative stress has been associated with the observed neurochemical changes in this disease. We evaluated the effects of gallic acid on hyperlocomotion, acetylcholinesterase activity, and oxidative stress in an animal model of ketamine-induced mania. Rats were pretreated orally with vehicle, gallic acid (50 or 100 mg/kg), or lithium (45 mg/kg twice a day) for 14 days. Between days 8 and 14, the animals also received ketamine (25 mg/kg) or saline daily. On the 15th day, hyperlocomotion was assessed, following which the animals were euthanized, and brains were collected. Results showed that ketamine induced hyperlocomotion and caused oxidative damage by increasing reactive oxygen species levels, lipid peroxidation, and nitrite levels, and decreasing the total thiol content and the activities of catalase, superoxide dismutase, and glutathione peroxidase in the brain. Pretreatment with gallic acid and lithium prevented hyperlocomotion and brain oxidative damage. Further, ketamine increased the acetylcholinesterase activity in the hippocampus and striatum, whereas gallic acid and lithium ameliorated this alteration. Thus, gallic acid may provide effective protection against manic-like behavior by reducing oxidative stress and preventing cholinergic signaling dysfunction in the brain regions involved in emotion regulation.
ESTHER : Recart_2021_Int.J.Dev.Neurosci__
PubMedSearch : Recart_2021_Int.J.Dev.Neurosci__
PubMedID: 33394512

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 : Alterations of ectonucleotidases and acetylcholinesterase activities in lymphocytes of Down syndrome subjects: Relation with inflammatory parameters - Rodrigues_2014_Clin.Chim.Acta_433C_105
Author(s) : Rodrigues R , Debom G , Soares F , Machado C , Pureza J , Peres W , de Lima Garcias G , Duarte MF , Schetinger MR , Stefanello F , Braganhol E , Spanevello R
Ref : Clinica Chimica Acta , 433C :105 , 2014
Abstract : BACKGROUND: Subjects with Down syndrome (DS) have an increased susceptibility to infections and autoimmune disorders. ATP, adenosine, and acetylcholine contribute to the immune response regulation, and NTPDase, adenosine deaminase (ADA) and acetylcholinesterase (AChE) are important enzymes in the control of the extracellular levels of these molecules. We evaluated the activities of these enzymes and the cytokine levels in samples of DS individuals.
METHODS: The population consisted of 23 subjects with DS and 23 healthy subjects. Twelve milliliters of blood was obtained from each subject and used for lymphocyte and serum preparation. Lymphocytes were separated on Ficoll density gradients. After isolation, NTPDase and AChE activities were determined.
RESULTS: The NTPDase activity using ADP as substrate was increased in lymphocytes of DS patients compared to control (P<0.05); however, no alterations were observed in the ATP hydrolysis. An increase was observed in the AChE activity in lymphocytes and in ADA activity in serum of DS patients when compared to healthy subjects (P<0.05). In DS subjects, an increase in the levels of IL-1beta, IL-6, TNF-alpha and IFN-gamma and a decrease in the IL-10 levels were also observed (P<0.05).
CONCLUSIONS: Alterations in the NTPDase, ADA and AChE activities as well changes in the cytokine levels may contribute to immunological alterations observed in DS.
ESTHER : Rodrigues_2014_Clin.Chim.Acta_433C_105
PubMedSearch : Rodrigues_2014_Clin.Chim.Acta_433C_105
PubMedID: 24631131

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 : 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 : 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 : Influence of Trypanosoma evansi in blood, plasma, and brain cholinesterase of experimentally infected cats - Da Silva_2010_Res.Vet.Sci_88_281
Author(s) : Da Silva AS , Spanevello R , Stefanello N , Wolkmer P , Costa MM , Zanette RA , Lopes ST , Santurio JM , Schetinger MR , Monteiro SG
Ref : Res Vet Sci , 88 :281 , 2010
Abstract : Changes in blood, plasma and brain cholinesterase activities in Trypanosoma evansi-infected cats were investigated. Seven animals were infected with 10(8) trypomastigote forms each and six were used as control. Animals were monitored for 56 days by examining daily blood smears. Blood samples were collected at days 28 and 56 post-inoculation to determine the activity of acetylcholinesterase (AChE) in blood and the activity of butyrylcholinesterase (BChE) in plasma. AChE was also evaluated in total brain. The activity of AChE in blood and brain, and the activity of BChE in plasma significantly reduced in the infected cats. Therefore, the infection by T. evansi influenced cholinesterases of felines indicating changes in the responses of the cholinergic system.
ESTHER : Da Silva_2010_Res.Vet.Sci_88_281
PubMedSearch : Da Silva_2010_Res.Vet.Sci_88_281
PubMedID: 19781725

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 : Metabolic and histological parameters of silver catfish (Rhamdia quelen) exposed to commercial formulation of 2,4-dichlorophenoxiacetic acid (2,4-D) herbicide - Cattaneo_2008_Pestic.Biochem.Physiol_92_133
Author(s) : Cattaneo R , Loro VL , Spanevello R , Silveira FA , Luz L , Miron DS , Fonseca MB , Moraes BS , Clasen B
Ref : Pesticide Biochemistry and Physiology , 92 :133 , 2008
Abstract : The objective of this study was to investigate the effects of commercial formulation of herbicide 2,4-D on metabolic parameters, acetylcholinesterase (AChE) activity and liver histological evaluation of silver catfish (Rhamdia quelen) exposed for 96 h. AChE activity increased in brain (600 and 700 mg L-1) and decreased in all concentrations tested in muscle tissue. Hepatic glycogen was reduced after 2,4-D exposure ranging from 47.67% (400 mg L-1) until 59.3% (700 mg L-1). Hepatic tissue showed lactate reduction at all 2,4-D concentrations tested and glucose was reduced only at 700 mg L-1. In the highest concentration tested hepatic glycogen and glucose reduced instead plasma glucose levels increased. White muscle tissue showed glycogen reduction in fingerlings exposed to all herbicide concentrations and glucose reduction at 700 mg L-1. Muscle lactate levels increase at all 2,4-D concentrations tested. Vacuolation of hepatocytes and changes in its arrangement cords were observed by histologic analysis in group treated with 700 mg/L of 2,4-D. These results suggest that silver catfish exposed to concentrations of 2,4-D near of CL50 showed metabolic and histological response to compensate some stress caused by herbicide exposure. Taken together parameters measured can be used as biomarkers to monitor herbicide contaminated water.
ESTHER : Cattaneo_2008_Pestic.Biochem.Physiol_92_133
PubMedSearch : Cattaneo_2008_Pestic.Biochem.Physiol_92_133
PubMedID:

Title : Effect of clomazone herbicide on biochemical and histological aspects of silver catfish (Rhamdia quelen) and recovery pattern - Crestani_2007_Chemosphere_67_2305
Author(s) : Crestani M , Menezes C , Glusczak L , dos Santos Miron D , Spanevello R , Silveira A , Goncalves FF , Zanella R , Loro VL
Ref : Chemosphere , 67 :2305 , 2007
Abstract : The effects of the herbicide, clomazone, on acetylcholinesterase (AChE), catalase and TBARS formation in teleost fish (Rhamdia quelen) were studied. The fish were exposed to 0.5 or 1.0 mg L(-1) of clomazone for 12, 24, 48, 96 and 192 h. After 192 h of exposure period, fish were transferred to clean water and kept in the same for 192 h to study the recovery response. Same parameters as that of exposure period were assayed after 96 and 192 h of recovery period. Specific AChE activity was reduced in the brain and muscle after treatments, reaching a maximum inhibition of 47% in the brain and 45% in the muscle after 12h of exposure. Fish exposed to clomazone increased TBARS production in the liver for all exposure periods. The brain presented elevated TBARS levels after 12, 24 and 48 h, but after 96 and 192 h, these levels decreased. The decrease of TBARS levels persisted in brain tissue after 96 h of recovery and returned to the control value after 192 h in clean water. Catalase activity was reduced for all periods of exposure. Histological analysis showed vacuolation in the liver after herbicide exposure. Some of the alterations observed were completely restored after recovery period.
ESTHER : Crestani_2007_Chemosphere_67_2305
PubMedSearch : Crestani_2007_Chemosphere_67_2305
PubMedID: 17280706

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