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1.
J Ethnopharmacol ; 264: 113139, 2021 Jan 10.
Artigo em Inglês | MEDLINE | ID: mdl-32726679

RESUMO

ETHNOPHARMACOLOGICAL RELEVANCE: Inflammatory skin diseases presents high prevalence and lack of alternatives that can be used for self-care by the population. Casearia sylvestris is a plant used topically in different communities in Brazil, to treat wounds or promote cutaneous healing. To evaluate the topical anti-inflammatory activity for the crude hydroalcoholic extract of Casearia sylvestris (HCE-CS) in the models of single or multiple administration of chroton oil to induce ear edema in mice. MATERIALS AND METHODS: Experimental study using male Swiss mice (25-35g) kept under constant conditions in the Laboratory of Experimental Neuroscience (LaNEx)-UNISUL. Edema was induced in both models, respectively, by the single or multiple application of croton oil (CO, 2.5%, in 20 µl) on the external surface of the ear. The different groups of animals (n = 8) received different treatments: vehicle, dexamethasone (DEXA) or different doses of HCE-CS. Edema was evaluated macroscopically for 6 h (early edema) or 8 days (late edema) after the first application of the CO and immediately after the animals were submitted to euthanasia for the collection of the samples (treated ears). For early edema, the tissue was biochemically evaluated for myeloperoxidase activity (MPO) and levels of nitrite/nitrate. In the late edema model, the ears were histologically evaluated for general morphometry, degranulated and non-degranulated mast cells, as well as acanthosis. RESULTS: Topic treatment with HCE-CS significantly reduced the early and late edema, as well as MPO activity and tissue levels of nitrite/nitrate. Finally, in the late edema model there was a lower density of degranulated mast cells in relation to the vehicle treated group and decreased thickness of the epidermis (acanthosis). CONCLUSION: These results suggest a possible benefit of topical treatment with HCE-CS in inflammatory conditions of the skin.

2.
J Biomater Appl ; 29(5): 654-61, 2014 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-25015652

RESUMO

This study reports the results of the characterization of cellulose acetate butyrate and polycaprolactone-triol blends in terms of miscibility, swelling capacity, mechanical properties, and inflammatory response in vivo. The cellulose acetate butyrate film was opaque and rigid, with glass transition (T g ) at 134℃ and melting temperature of 156℃. The cellulose acetate butyrate/polycaprolactone-triol films were transparent up to a polycaprolactone-triol content of 60%. T g of the cellulose acetate butyrate films decreased monotonically as polycaprolactone-triol was added to the blend, thus indicating miscibility. FTIR spectroscopy revealed a decrease in intramolecular hydrogen bonding in polycaprolactone-triol, whereas no hydrogen bonding was observed between cellulose acetate butyrate and -OH from polycaprolactone-triol. The increase in polycaprolactone-triol content in the blend decreased the water uptake. An increase in polycaprolactone-triol content decreased the modulus of elasticity and increased the elongation at break. A cellulose acetate butyrate/polycaprolactone-triol 70/30 blend implanted in rats showed only an acute inflammatory response 7 days after surgery. No change in inflammation mediators was observed.


Assuntos
Materiais Biocompatíveis/química , Celulose/análogos & derivados , Poliésteres/química , Animais , Técnicas Biossensoriais , Varredura Diferencial de Calorimetria , Celulose/química , Sistemas de Liberação de Medicamentos , Elasticidade , Ligação de Hidrogênio , Inflamação , Masculino , Teste de Materiais , Ratos , Ratos Wistar , Espectrofotometria Infravermelho , Espectroscopia de Infravermelho com Transformada de Fourier , Estresse Mecânico , Temperatura , Resistência à Tração
3.
Metab Brain Dis ; 26(2): 115-22, 2011 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-21437673

RESUMO

Contrast-induced nephropathy is a common cause of acute renal failure in hospitalized patients, occurring from 24 to 48 h and up to 5 days after the administration of iodinated contrast media. Encephalopathy may accompany acute renal failure and presents with a complex of symptoms progressing from mild sensorial clouding to delirium and coma. The mechanisms responsible for neurological complications in patients with acute renal failure are still poorly known, but several studies suggest that mitochondrial dysfunction plays a crucial role in the pathogenesis of uremic encephalopathy. Thus, we measured mitochondrial respiratory chain complexes and creatine kinase activities in rat brain and kidney after administration of contrast media. Wistar rats were submitted to 6.0 ml/kg meglumine/sodium diatrizoate administration via the tail vein (acute renal failure induced by contrast media) and saline in an equal volume with the radiocontrast material (control group); 6 days after, the animals were killed and kidney and brain were obtained. The results showed that contrast media administration decreased complexes I and IV activities in cerebral cortex; in prefrontal cortex, complex I activity was inhibited. On the other hand, contrast media administration increased complexes I and II-III activities in hippocampus and striatum and complex IV activity in hippocampus. Moreover, that administration of contrast media also decreased creatine kinase activity in the cerebral cortex. The present findings suggest that the inhibition of mitochondrial respiratory chain complexes and creatine kinase caused by the acute renal failure induced by contrast media administration may be involved in the neurological complications reported in patients and might play a role in the pathogenesis of the encephalopathy caused by acute renal failure.


Assuntos
Encefalopatias Metabólicas , Meios de Contraste , Creatina Quinase/metabolismo , Complexo de Proteínas da Cadeia de Transporte de Elétrons/metabolismo , Metabolismo Energético/fisiologia , Nefropatias , Animais , Encéfalo/enzimologia , Encefalopatias Metabólicas/etiologia , Encefalopatias Metabólicas/patologia , Meios de Contraste/administração & dosagem , Meios de Contraste/efeitos adversos , Creatinina/sangue , Modelos Animais de Doenças , Humanos , Rim/metabolismo , Nefropatias/induzido quimicamente , Nefropatias/complicações , Mitocôndrias/metabolismo , Estresse Oxidativo , Ratos , Ratos Wistar
4.
Basic Clin Pharmacol Toxicol ; 108(3): 214-9, 2011 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-21138529

RESUMO

The pathophysiology of gastritis involves an imbalance between gastric acid attack and mucosal defence. In addition, the gastric mucosal injury results in adenosine triphosphate (ATP) depletion leading to mitochondrial dysfunction. Several studies have shown the association of mitochondrial disorders with gastrointestinal dysfunction. In the present study, we investigated the activity of mitochondrial respiratory chain complexes activity in the stomach of rats with gastritis induced by indomethacin (IDM) and treated with omeprazole (OM), N-acetylcysteine (NAC) and the gastrin-releasing peptide receptor (GRPR) antagonist RC-3095. Adult male Wistar rats were pre-treated for 7 days with OM, NAC, RC-3095, combination of OM plus RC-3095, OM plus NAC and water (control). The animals were then submitted to fasting for 24 hr; IDM was administered. The rats were killed 6 hr later, and the stomachs were used for evaluation of macroscopic damage and respiratory chain activity. Our results showed that complex I and IV activities were not affected by administration of IDM. On the other hand, complex II and III activities were inhibited. In addition, OM plus RC-3095 and OM plus NAC did not reverse complex II activity inhibition. However, the complex III activity inhibition was reversed only with the combined use of OM plus RC-3095 and OM plus NAC. Our results are in agreement with previous studies indicating mitochondrial dysfunction in the pathophysiology of gastrointestinal tract disease and we suggest that GRPR antagonism might be a novel therapeutic strategy in gastritis.


Assuntos
Acetilcisteína/farmacologia , Antiulcerosos/farmacologia , Bombesina/análogos & derivados , Complexo II de Transporte de Elétrons/metabolismo , Gastrite/metabolismo , Omeprazol/farmacologia , Fragmentos de Peptídeos/farmacologia , Receptores da Bombesina/antagonistas & inibidores , Acetilcisteína/uso terapêutico , Animais , Anti-Inflamatórios não Esteroides/toxicidade , Antiulcerosos/uso terapêutico , Bombesina/farmacologia , Bombesina/uso terapêutico , Quimioterapia Combinada , Transporte de Elétrons/efeitos dos fármacos , Complexo II de Transporte de Elétrons/antagonistas & inibidores , Complexo III da Cadeia de Transporte de Elétrons/antagonistas & inibidores , Complexo III da Cadeia de Transporte de Elétrons/metabolismo , Mucosa Gástrica/metabolismo , Gastrite/patologia , Gastrite/prevenção & controle , Indometacina/toxicidade , Masculino , Mitocôndrias/efeitos dos fármacos , Mitocôndrias/enzimologia , Omeprazol/uso terapêutico , Fragmentos de Peptídeos/uso terapêutico , Inibidores da Bomba de Prótons/farmacologia , Inibidores da Bomba de Prótons/uso terapêutico , Ratos , Ratos Wistar , Índice de Gravidade de Doença , Estômago/efeitos dos fármacos , Estômago/patologia , Úlcera Gástrica/prevenção & controle
5.
Neurochem Res ; 35(4): 515-21, 2010 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-20238483

RESUMO

The pathogenesis of sepsis is characterized by an overwhelming systemic inflammatory response that can lead to multiple organ failure. Considering that we have recently demonstrated that mitochondrial respiratory chain and creatine kinase (CK) are altered in the brain of rats after cecal ligation and perforation (CLP) and that a combination of N-acetylcysteine/deferoxamine (NAC/DFX), taurine and RC-3095 were shown to be an effective treatment of sepsis, we investigated whether the alterations of these enzymes may be reversed by these drugs. The results demonstrated that CLP inhibited complexes I and II, and that all the treatments were able to reverse this inhibition in all brain areas studied in the present work. On the other hand, complexes III and IV were not affected by sepsis neither by any of the treatments. An increase in CK activity in brain of rats 12 h after CLP was also verified; the administration of NAC/DFX and taurine reversed the increase in CK activity in hippocampus, cerebral cortex, cerebellum and striatum. On the other hand, RC-3095 significantly decreased CK activity, when compared to sham group in all brain areas studied. This is a preliminary study which showed beneficial effects of the treatments we proposed.


Assuntos
Acetilcisteína/farmacologia , Bombesina/análogos & derivados , Encéfalo/efeitos dos fármacos , Creatina Quinase/metabolismo , Desferroxamina/farmacologia , Transporte de Elétrons/efeitos dos fármacos , Fragmentos de Peptídeos/farmacologia , Sepse/metabolismo , Taurina/farmacologia , Animais , Bombesina/farmacologia , Encéfalo/enzimologia , Encéfalo/metabolismo , Masculino , Ratos , Ratos Wistar , Sepse/enzimologia
6.
Mitochondrion ; 8(4): 313-8, 2008 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-18657632

RESUMO

The mechanisms responsible to the development of brain dysfunction during sepsis are not well understood. The objective of this study is to evaluate mitochondrial respiratory chain and creatine kinase activities in the brain after cecal ligation and perforation (CLP) in rats. We performed a prospective, controlled experiment in male Wistar rats. Rats were subjected to CLP (sepsis group) with saline resuscitation (at 50mL/kg immediately and 12h after cecal ligation and perforation) or sham operation (control group). Several times (0, 6, 12, 24, 48 and 96h) after CLP six rats were killed by decapitation, and brain structures (cerebellum, hippocampus, striatum and cortex) were isolated. Mitochondrial respiratory chain and creatine kinase activity were then measured. It was observed that animals submitted to CLP presented decreased mitochondrial respiratory chain activity in complex I, but not in complex II, III and IV, 24, 48 and 96h in all analyzed structures. Activity of succinate dehydrogenase was decreased in 48 and 96h in all analyzed structures. Creatine kinase activity increased after CLP in cerebellum, hippocampus and cortex (after 0h) and striatum (after 6h). Sepsis associated brain injury may include dysfunction in the mitochondrial respiratory chain activity.


Assuntos
Creatina Quinase/metabolismo , Transporte de Elétrons , Mitocôndrias/fisiologia , Sepse/fisiopatologia , Animais , Encéfalo/enzimologia , Ceco/fisiologia , Transporte de Elétrons/efeitos dos fármacos , Ligadura , Masculino , Atividade Motora , Ratos , Ratos Wistar , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
7.
Prog Neuropsychopharmacol Biol Psychiatry ; 32(4): 1064-8, 2008 May 15.
Artigo em Inglês | MEDLINE | ID: mdl-18403082

RESUMO

Studies have consistently reported the participation of free radicals in Bipolar Disorder. Administration of d-amphetamine (d-AMPH) is a relevant animal model of mania and it increases oxidative stress in rat brain. Evidences indicate that the antioxidants N-acetylcysteine (NAC) and Deferoxamine (DFX) exert protective effects in the brain. The present study was designed to evaluate the effects of NAC, DFX or their combination on AMPH-induced hyperactivity. The protein oxidation levels were analyzed in prefrontal cortex and hippocampus. In the first animal model (reversal treatment), adult male Wistar rats received saline or d-AMPH for 14 days, and from the 8th to the 14th day, they were treated with saline, NAC, DFX, or NAC plus DFX. In the second animal model (prevention treatment), rats were pretreated with saline or antioxidant regime, and from the 8th to the 14th day, they also received saline or d-AMPH. In the prefrontal cortex, the protein carbonyls were not affected by the treatment with antioxidants alone but it was increased by treatment with NAC plus DFX. At the same model, NAC plus DFX reversed the protein damage in the hippocampus, but NAC alone increased this damage. In the prevention treatment, it was observed that the protein damage in the prefrontal cortex was prevented by DFX or NAC plus DFX. In the hippocampus, the pretreatment with all antioxidant regime prevented protein damage induced by d-AMPH. At both treatments (reversal or prevention) the antioxidants did not present any effect against d-AMPH-induced hyperactivity. In conclusion, NAC or DFX and the combination of NAC plus DFX reverse and protect against d-AMPH-induced oxidative protein damage. Using these protocols we could not observe affects on locomotion, however this effect varies depending on the brain region and the treatment regime.


Assuntos
Acetilcisteína/farmacologia , Transtorno Bipolar/induzido quimicamente , Transtorno Bipolar/psicologia , Desferroxamina/farmacologia , Depuradores de Radicais Livres/farmacologia , Hipercinese/induzido quimicamente , Hipercinese/psicologia , Estresse Oxidativo/efeitos dos fármacos , Animais , Estimulantes do Sistema Nervoso Central/farmacologia , Dextroanfetamina/farmacologia , Hipercinese/prevenção & controle , Masculino , Carbonilação Proteica/efeitos dos fármacos , Ratos , Ratos Wistar
8.
Neurotox Res ; 13(1): 63-9, 2008 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-18367441

RESUMO

Typical and atypical antipsychotic drugs have been shown to have different clinical and behavioral profiles. Haloperidol (HAL) is a typical neuroleptic that acts primarily as a D(2) dopamine receptor antagonist. It has been proposed that reactive oxygen species play a causative role in neurotoxic effects induced by HAL. We evaluated oxidative damage in rat brain induced by chronic (28 days) HAL, clozapine (CLO), olanzapine (OLZ) or aripiprazole (ARI) administration. Adult male Wistar rats received daily injections of HAL (1.5 mg/kg), CLO (25 mg/kg), OLZ (2.5, 5 or 10 mg/kg) or ARI (2, 10 or 20 mg/kg); control animals received vehicle (Tween 1% solution). Thiobarbituric acid reactive substances (TBARS) and protein carbonylation were measured in the prefrontal cortex, hippocampus, striatum and cerebral cortex. The results showed that TBARS were increased in the striatum after HAL treatment. On the other hand, TBARS were diminished in the prefrontal cortex by OLZ and ARI. Our results also showed that all drugs tested in this work decreased TBARS levels in the cerebral cortex. In hippocampus, TBARS levels were not altered by any drug. Protein carbonyl content after HAL and CLO treatment was increased in the hippocampus. Moreover, OLZ and ARI did not alter protein carbonyl content when compared to control group. ARI chronic administration (20 mg/kg) also increased mitochondrial superoxide in the prefrontal cortex and striatum. ARI did not alter mitochondrial superoxide in the hippocampus and cerebral cortex. Moreover, HAL, OLZ and CLO did not cause significant alterations in mitochondrial superoxide in rat brain. Our findings demonstrate that OLZ and ARI do not induce oxidative damage in rat brain as observed after HAL and CLO treatment.


Assuntos
Antipsicóticos/toxicidade , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Haloperidol/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Animais , Aripiprazol , Benzodiazepinas/toxicidade , Clozapina/toxicidade , Corpo Estriado/efeitos dos fármacos , Corpo Estriado/metabolismo , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Masculino , Olanzapina , Piperazinas/toxicidade , Córtex Pré-Frontal/efeitos dos fármacos , Córtex Pré-Frontal/metabolismo , Quinolonas/toxicidade , Ratos , Ratos Wistar , Superóxidos/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
9.
Neurochem Res ; 33(6): 1024-7, 2008 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-18049893

RESUMO

Methylphenidate (MPH) is psychostimulants used to treat Attention-Deficit/Hyperactivity Disorder and can lead to a long-lasting neurochemical and behavioral adaptations in experimental animals. In the present study, the cerebral antioxidant enzymatic system, superoxide dismutase (SOD) and catalase (CAT) was evaluated at in different age following MPH (1, 2 or 10 mg/kg MPH, i.p.) treatment in young rats. In the acute treatment the SOD activity decreased in the cerebral prefrontal cortex with opposite effect in the cerebral cortex; and the CAT activity decreased in hippocampus. In the chronic treatment the SOD activity increased in the hippocampus and cerebral cortex and decreased in the striatum. The observed changes on the enzyme activities in rat brain were dependent on the structure brain region and duration of treatment with MPH. Probably, the activity of enzymes was not be enough to prevent MPH-induced oxidative damage in specific regions from brain, such as observed for us in another recent study.


Assuntos
Antioxidantes/metabolismo , Catalase/metabolismo , Estimulantes do Sistema Nervoso Central/metabolismo , Metilfenidato/metabolismo , Superóxido Dismutase/metabolismo , Animais , Encéfalo/anatomia & histologia , Encéfalo/efeitos dos fármacos , Encéfalo/enzimologia , Estimulantes do Sistema Nervoso Central/farmacologia , Isoenzimas/metabolismo , Masculino , Metilfenidato/farmacologia , Ratos , Ratos Wistar
10.
J Psychiatry Neurosci ; 31(5): 326-32, 2006 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-16951735

RESUMO

OBJECTIVE: Previous studies have suggested that oxidative stress may play a role in the pathophysiology of bipolar disorder (BD). Moreover, recent studies indicate that lithium and valproate exert neuroprotective effects against oxidative stress. We studied the effects of the mood stabilizers lithium and valproate on amphetamine-induced oxidative stress in an animal model of mania. METHODS: In the first model (reversal treatment), adult male Wistar rats received d-amphetamine or saline for 14 days, and between the 8th and 14th days, they were treated with lithium, valproate or saline. In the second model (prevention treatment), rats were pretreated with lithium, valproate or saline, and between the 8th and 14th days, they received d-amphetamine or saline. We assessed locomotor activity with the open-field task. We measured thiobarbituric acid reactive substances (TBARS) and protein carbonyl formation, as parameters of oxidative stress, and superoxide dismutase (SOD) and catalase (CAT), the major antioxidant enzymes, in the prefrontal cortex and hippocampus. RESULTS: Lithium and valproate reversed (reversal treatment model) and prevented (prevention treatment model) amphetamine-induced hyperactivity and reversed and prevented amphetamine-induced TBARS formation in both experiments. However, the co-administration of lithium or valproate with amphetamine increased lipid peroxidation, depending on the brain region and treatment regimen. No changes in protein carbonyl formation were observed. SOD activity varied with different treatment regimens, and CAT activity increased when the index of lipid peroxidation was more robust. CONCLUSION: Our findings suggest that lithium and valproate exert protective effects against amphetamine-induced oxidative stress in vivo, further supporting the hypothesis that oxidative stress may be associated with the pathophysiology of BD.


Assuntos
Anticonvulsivantes/farmacologia , Antimaníacos/farmacologia , Transtorno Bipolar/fisiopatologia , Modelos Animais de Doenças , Carbonato de Lítio/farmacologia , Estresse Oxidativo/efeitos dos fármacos , Ácido Valproico/farmacologia , Animais , Transtorno Bipolar/induzido quimicamente , Catalase/metabolismo , Dextroanfetamina , Interações Medicamentosas , Hipocampo/efeitos dos fármacos , Hipocampo/fisiopatologia , Peroxidação de Lipídeos/efeitos dos fármacos , Peroxidação de Lipídeos/fisiologia , Masculino , Atividade Motora/efeitos dos fármacos , Atividade Motora/fisiologia , Estresse Oxidativo/fisiologia , Córtex Pré-Frontal/efeitos dos fármacos , Córtex Pré-Frontal/fisiopatologia , Carbonilação Proteica/efeitos dos fármacos , Carbonilação Proteica/fisiologia , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
11.
Neurochem Res ; 31(5): 671-8, 2006 May.
Artigo em Inglês | MEDLINE | ID: mdl-16770738

RESUMO

Malathion is a pesticide with high potential for human exposure. However, it is possible that during the malathion metabolism, there is generation of reactive oxygen species (ROS) and malathion may produce oxidative stress in intoxicated rats. The present study was therefore undertaken to determine malathion-induced lipid peroxidation (LPO), protein carbonylation and to determine whether malathion intoxication alters the antioxidant system in brain rats. Malathion was administered intraperitoneally in the acute and chronic protocols in the doses of 25, 50, 100 and 150 mg malathion/kg. The results showed that LPO in brain increased in both protocols. The increased oxidative stress resulted in an increased in the activity of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT), observed in cortex, striatum in the acute malathion protocol and hippocampus in the chronic malathion protocol. Our results demonstrated that malathion induced oxidative stress and modulated SOD and CAT activity in selective brain regions.


Assuntos
Encéfalo/metabolismo , Inibidores da Colinesterase/metabolismo , Malation/metabolismo , Estresse Oxidativo , Animais , Encéfalo/anatomia & histologia , Catalase/metabolismo , Humanos , Masculino , Ratos , Ratos Wistar , Superóxido Dismutase/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
12.
Neurochem Res ; 31(5): 699-703, 2006 May.
Artigo em Inglês | MEDLINE | ID: mdl-16770742

RESUMO

Studies have demonstrated that oxidative stress is associated with amphetamine-induced neurotoxicity, but little is known about the adaptations of antioxidant enzymes in the brain after amphetamine exposure. We studied the effects of acute and chronic amphetamine administration on superoxide dismutase (SOD) and catalase (CAT) activity, in a rodent model of mania. Male Wistar rats received either a single IP injection of D-: amphetamine (1 mg/kg, 2 mg/kg, or 4 mg/kg) or vehicle (acute treatment). In the chronic treatment rats received a daily IP injection of either D-: amphetamine (1 mg/kg, 2 mg/kg, or 4 mg/kg) or vehicle for 7 days. Locomotor behavior was assessed using the open field test. SOD and CAT activities were measured in the prefrontal cortex, hippocampus, and striatum. Acute and to a greater extent chronic amphetamine treatment increased locomotor behavior and affected SOD and CAT activities in the prefrontal cortex, hippocampus and striatum. Our findings suggest that amphetamine exposure is associated with an imbalance between SOD and CAT activity in the prefrontal cortex, hippocampus and striatum.


Assuntos
Anfetamina/metabolismo , Antioxidantes/metabolismo , Transtorno Bipolar/metabolismo , Catalase/metabolismo , Dopaminérgicos/metabolismo , Superóxido Dismutase/metabolismo , Anfetamina/administração & dosagem , Animais , Encéfalo/anatomia & histologia , Encéfalo/metabolismo , Dopaminérgicos/administração & dosagem , Masculino , Ratos , Ratos Wistar
13.
Prog Neuropsychopharmacol Biol Psychiatry ; 30(7): 1231-4, 2006 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-16631293

RESUMO

INTRODUCTION: Psychostimulants such as amphetamine (AMPH) induce manic-like symptoms in humans and studies have suggested that bipolar disorder (BD) may be associated to dopamine dysfunction. Glial fibrillary acidic protein (GFAP) up-regulation is considered a marker of astrogliosis, and it has been associated to behavioral sensitization. PURPOSE: We aimed to investigate the behavioral effects of acute and chronic AMPH on rat locomotion and assess GFAP levels in rat cortex and hippocampus. METHODS: Rats were administered either acute (single dose) or chronic (seven days) d-amphetamine IP injection. Locomotion was assessed with an open-field test and GFAP immunoquantity was measured using ELISA. RESULTS: Chronic, but not acute, administration of AMPH increased GFAP levels in rat hippocampus. No differences were observed in rat cortex. CONCLUSIONS: Repeated exposure to AMPH leads to an astroglial response in the hippocampus of rats.


Assuntos
Astrócitos/efeitos dos fármacos , Estimulantes do Sistema Nervoso Central/administração & dosagem , Dextroanfetamina/administração & dosagem , Hipocampo/citologia , Hipocampo/efeitos dos fármacos , Análise de Variância , Animais , Comportamento Animal/efeitos dos fármacos , Córtex Cerebral/efeitos dos fármacos , Córtex Cerebral/metabolismo , Relação Dose-Resposta a Droga , Esquema de Medicação , Ensaio de Imunoadsorção Enzimática/métodos , Expressão Gênica/efeitos dos fármacos , Proteína Glial Fibrilar Ácida/efeitos dos fármacos , Hipocampo/metabolismo , Imuno-Histoquímica/métodos , Masculino , Atividade Motora/efeitos dos fármacos , Ratos , Ratos Wistar
14.
Brain Res ; 1078(1): 189-97, 2006 Mar 17.
Artigo em Inglês | MEDLINE | ID: mdl-16494852

RESUMO

Methylphenidate (MPH) is frequently prescribed for the treatment of attention deficit/hyperactivity disorder. Psychostimulants can cause long-lasting neurochemical and behavioral adaptations. Here, we evaluated oxidative damage in the rat brain and the differential age-dependent response to MPH after acute and chronic exposure. We investigated the oxidative damage, assessed by the thiobarbituric acid reactive species (TBARS), and the protein carbonyl assays in cerebellum, prefrontal cortex, hippocampus, striatum, and cerebral cortex of young (25 days old) and adult (60 days old) male Wistar rats after acute and chronic exposure to MPH. Chronic MPH-treated young rats presented a dose-dependent increase in TBARS content and protein carbonyls formation in specific rat brain regions. In the acute exposure, only MPH highest dose increased lipid peroxidation in the hippocampus. No difference in protein carbonylation was observed among groups in all structures analyzed. In adult rats, we did not find oxidative damage in both acute and chronic treatment. Chronic exposure to MPH in induces oxidative damage in young rat brain, differentially from chronic exposure during adulthood. These findings highlight the need for further research to improve understanding of MPH effects on developing nervous system and the potential consequences in adulthood resulting from early-life drug exposure.


Assuntos
Química Encefálica/efeitos dos fármacos , Encéfalo/efeitos dos fármacos , Estimulantes do Sistema Nervoso Central/administração & dosagem , Metilfenidato/administração & dosagem , Estresse Oxidativo/efeitos dos fármacos , Fatores Etários , Análise de Variância , Animais , Animais Recém-Nascidos , Relação Dose-Resposta a Droga , Esquema de Medicação , Masculino , Carbonilação Proteica/efeitos dos fármacos , Ratos , Ratos Wistar , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
15.
Neurotox Res ; 9(1): 23-8, 2006 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-16464749

RESUMO

Lipid peroxidation is one of the major outcomes of free radical-mediated injury to tissue in vivo, including the central nervous system (CNS). The aim of this study was to examine whether malathion, a commonly used organophosphorus (OP), might induce oxidative stress in cerebrospinal fluid, blood serum and brain structures in male Wistar rats. Malathion was administered intraperitoneally in the doses of 25, 50, 100 and 150 mg/kg for 28 days. Oxidative damage was determined by measuring the thiobarbituric acid reactive species (TBARS) content, as an index of lipid peroxidation. TBARS concentration in the cerebrospinal fluid (CSF) and brain structures were increased, but a decrease in TBARS concentration in serum was observed. The results of the present study suggest the usefulness of TBARS measurement as a good biomarker in the estimation of malathion-induced oxidative stress affecting CSF and brain structures.


Assuntos
Encéfalo/efeitos dos fármacos , Inibidores da Colinesterase/toxicidade , Peroxidação de Lipídeos/efeitos dos fármacos , Malation/toxicidade , Análise de Variância , Animais , Relação Dose-Resposta a Droga , Esquema de Medicação , Masculino , Ratos , Ratos Wistar , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Distribuição Tecidual/efeitos dos fármacos
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