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1.
Microb Pathog ; 138: 103817, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31672529

RESUMO

Flavobacterium columnare, the causative agent of columnaris disease, is a serious bacterial disease responsible for causing devastating mortality rates in several species of freshwater fish, leading to severe economic losses in the aquaculture industry. Notwithstanding the enormous impacts this disease can have, very little is known regarding the interaction between the host and bacterium in terms of the mortality rate of silver catfish (Rhamdia quelen), as well its linkage to gill energetic homeostasis. Therefore, we conducted independent experiments to evaluate the mortality rates caused by F. columnare in silver catfish, as well as whether columnaris disease impairs the enzymes of the phosphoryl transfer network in gills of silver catfish and the pathways involved in this inhibition. Experiment I revealed that clinical signs started to appear 72 h post-infection (hpi), manifesting as lethargy, skin necrosis, fin erosion and gill discoloration. Silver catfish began to die at 96 hpi, and 100% mortality was observed at 120 hpi. Experiment II revealed that creatine kinase (CK, cytosolic and mitochondrial) and pyruvate kinase (PK) activities were inhibited in silver catfish experimentally infected with F. columnare, while no significant difference was observed between experimental and control groups with respect to adenylate kinase activity. Activity of the branchial sodium-potassium pump (Na+, K+-ATPase) was inhibited while reactive oxygen species (ROS) and lipid peroxidation levels were higher in silver catfish experimentally infected with F. columnare than in the control group at 72 hpi. Based on these data, the impairment of CK activity elicited by F. columnare caused a disruption in branchial energetic balance, possibly reducing ATP availability in the gills and provoking impairment of Na+, K +ATPase activity. The inhibition of CK and PK activities appears to be mediated by ROS overproduction and lipid peroxidation, both of which contribute to disease pathogenesis associated with branchial tissue.

2.
Microb Pathog ; 135: 103649, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31374321

RESUMO

Extracellular adenosine triphosphate (ATP) is as key mediator of immune and inflammatory responses. ATP is normally sequestered in the intracellular milieu and released by apoptotic and necrotic cells, where it acts as a pro-inflammatory mediator in the extracellular milieu. A limited number of studies have explored the involvement of purinergic signaling in oomycete infections, including Saprolegnia parasitica; this is a most destructive oomycete pathogen, associated with high mortality and severe economic losses for fish producers. The aim of this study was to determine whether purinergic signaling exerts anti- or pro-inflammatory effects in spleens of grass carp (Ctenopharyngodon idella) naturally infected by S. parasitica. Animals naturally infected with S. parasitica showed typical gross lesions characterized by cotton-wool tufts on the tail and fins, as well as severe histopathological lesions such as necrosis. Spleen ATP and metabolites of nitric oxide (NOx) levels were higher in fish naturally infected by S. parasitica compared to control on day 7 post-infection (PI). Spleen nucleoside triphosphate diphosphohydrolase (NTPDase) activity (ATP as substrate) was greater in fish naturally infected by S. parasitica than in uninfected on day 7 PI, while no significant differences were observed between groups with respect to NTPDase (adenosine diphosphate as substrate) and 5'-nucleotidase activities. Finally, adenosine deaminase (ADA) activity was lower in fish naturally infected by S. parasitica than in uninfected fish on day 7 PI. In summary, spleen tissue necrosis in the context of saprolegniosis provokes an intense release of ATP into the extracellular milieu, where it interacts with the P2X7 purine receptor and leads to a self-sustained pro-inflammatory deleterious cycle, contributing to an intense inflammatory process. In response to excessive ATP levels in the extracellular milieu, ATP and adenosine hydrolysis were modulated in an attempt to restrict the inflammatory process via upregulation of NTPDase and downregulation of ADA activities. We conclude that the purinergic signaling pathway modulates immune and inflammatory responses during natural infection with S. parasitica.


Assuntos
Trifosfato de Adenosina/metabolismo , Anti-Inflamatórios/metabolismo , Carpas/imunologia , Doenças dos Peixes/imunologia , Doenças dos Peixes/parasitologia , Purinérgicos/metabolismo , Transdução de Sinais , Baço/metabolismo , Adenosina Desaminase/metabolismo , Animais , Carpas/metabolismo , Modelos Animais de Doenças , Doenças dos Peixes/patologia , Proteínas de Peixes/imunologia , Micoses , Necrose , Óxido Nítrico/metabolismo , Saprolegnia/patogenicidade , Baço/patologia
3.
Microb Pathog ; 131: 164-169, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30978428

RESUMO

Bacterial diseases are one of the major problems in freshwater fish culture and have been linked to significant losses and high mortality rate. In this study, Nile tilapia Oreochromis niloticus was infected by Providencia rettgeri to evaluate the oxidative stress and antioxidant responses in the fish tissues. Juvenile Nile tilapia was divided into two groups, as follow: control (uninfected) and experimentally infected with 100 µL of P. rettgeri suspension containing 2.4 × 107 viable cells/fish, and the liver and kidney tissues were collected on days 7 and 14 post-infection (PI). Liver and kidney ROS and lipid peroxidation levels were high in infected fish on day 14 PI compared to control group, while superoxide dismutase activity was lower in liver (days 7 and 14 PI) and kidney (day 14 PI) compared to their respective control groups. Liver and kidney antioxidant capacity against peroxyl radicals, non-proteic, and proteic thiols levels was lower in infected tilapia on day 14 PI compared to control group. Based on these results, P. rettgeri infection may elicit oxidative damage via increased ROS production, decreased ROS elimination and inhibits enzymatic and non-enzymatic antioxidant defense systems; which may contribute directly to disease pathophysiology of infected animals.


Assuntos
Antioxidantes/metabolismo , Ciclídeos/metabolismo , Doenças dos Peixes/metabolismo , Estresse Oxidativo , Providencia/patogenicidade , Animais , Brasil , Ciclídeos/imunologia , Ciclídeos/microbiologia , Modelos Animais de Doenças , Infecções por Enterobacteriaceae/imunologia , Infecções por Enterobacteriaceae/microbiologia , Infecções por Enterobacteriaceae/veterinária , Doenças dos Peixes/imunologia , Doenças dos Peixes/microbiologia , Interações Hospedeiro-Patógeno/fisiologia , Rim/metabolismo , Peroxidação de Lipídeos , Fígado/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Tilápia/microbiologia
4.
Environ Toxicol Pharmacol ; 60: 45-51, 2018 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-29660609

RESUMO

It is known that the cytotoxic effects of aflatoxin B1 (AFB1) in endothelial cells of the blood-brain barrier (BBB) are associated with behavioral dysfunction. However, the effects of a diet contaminated with AFB1 on the behavior of silver catfish remain unknown. Thus, the aim of this study was to evaluate whether an AFB1-contaminated diet (1177 ppb kg feed-1) impaired silver catfish behavior, as well as whether disruption of the BBB and alteration of neurotransmitters in brain synaptosomes are involved. Fish fed a diet contaminated with AFB1 presented a behavioral impairment linked with hyperlocomotion on days 14 and 21 compared with the control group (basal diet). Neurotransmitter levels were also affected on days 14 and 21. The permeability of the BBB to Evans blue dye increased in the intoxicated animals compared with the control group, which suggests that the BBB was disrupted. Moreover, acetylcholinesterase (AChE) activity in brain synaptosomes was increased in fish fed a diet contaminated with AFB1, while activity of the sodium-potassium pump (Na+, K+-ATPase) was decreased. Based on this evidence, the present study shows that silver catfish fed a diet containing AFB1 exhibit behavioral impairments related to hyperlocomotion. This diet caused a disruption of the BBB and brain lesions, which may contribute to the behavioral changes. Also, the alterations in the activities of AChE and Na+, K+-ATPase in brain synaptosomes may directly contribute to this behavior, since they may promote synapse dysfunction. In addition, the hyperlocomotion may be considered an important macroscopic marker indicating possible AFB1 intoxication.


Assuntos
Aflatoxina B1/toxicidade , Ração Animal/toxicidade , Peixes-Gato/fisiologia , Neurotransmissores/metabolismo , Sinaptossomos/metabolismo , Acetilcolinesterase/metabolismo , Animais , Comportamento Animal/efeitos dos fármacos , Barreira Hematoencefálica/efeitos dos fármacos , Proteínas de Peixes/metabolismo , Contaminação de Alimentos , Regulação da Expressão Gênica/efeitos dos fármacos , ATPase Trocadora de Sódio-Potássio/metabolismo , Sinaptossomos/efeitos dos fármacos
5.
Microb Pathog ; 117: 157-161, 2018 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-29471134

RESUMO

The precise coupling of spatially separated intracellular adenosine triphosphate (ATP)-producing and ATP-consuming, catalyzed by creatine kinase (CK), adenylate kinase (AK), and pyruvate kinase (PK), is a critical process in the bioenergetics of tissues with high energy demand, such as the branchial tissue. The effects of Citrobacter freundii infection on gills remain poorly understood, limited only to histopathological studies. Thus, the aim of this study was to evaluate whether experimental infection by C. freundii impairs the enzymes of the phosphoryl transfer network in gills of silver catfish (Rhamdia quelen). The CK (cytosolic and mitochondrial) and AK activities decreased in infected compared to uninfected animals, while the PK activity did not differ between groups. The gill histopathology of infected animals revealed extensive degeneration with fusion and necrosis of secondary lamellae, detachment of superficial epithelium, aneurysm, vessel congestion and inflammatory process. Based on these evidences, the inhibition and absence of an efficient communication between CK compartments caused the impairment of the branchial bioenergetics homeostasis, which was not compensated by the augmentation on branchial AK activity in an attempt to restore energy homeostasis. In summary, these alterations contribute to disease pathogenesis linked to branchial tissue in animals infected with C. freundii.


Assuntos
Peixes-Gato/microbiologia , Citrobacter freundii/patogenicidade , Metabolismo Energético , Infecções por Enterobacteriaceae/metabolismo , Infecções por Enterobacteriaceae/veterinária , Doenças dos Peixes/metabolismo , Brânquias/enzimologia , Brânquias/metabolismo , Homeostase , Adenilato Quinase/metabolismo , Aneurisma/patologia , Animais , Região Branquial/patologia , Brasil , Creatina Quinase/metabolismo , Citosol/enzimologia , Modelos Animais de Doenças , Epitélio/patologia , Doenças dos Peixes/patologia , Brânquias/microbiologia , Brânquias/patologia , Hiperemia/patologia , Mitocôndrias/enzimologia , Necrose/patologia , Fosforilação , Piruvato Quinase/metabolismo , Virulência
6.
Mol Cell Biochem ; 443(1-2): 131-138, 2018 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-29086165

RESUMO

Appropriate control of the immune response is a critical determinant of fish health, and the purinergic cascade has an important role in the immune and inflammatory responses. This cascade regulates the levels of adenosine triphosphate (ATP), adenosine diphosphate, adenosine monophosphate and adenosine (Ado), molecules involved in physiological or pathological events as inflammatory and anti-inflammatory mediators. Thus, the aim of this study was to evaluate whether purinergic signaling, through the activities of nucleoside triphosphate diphosphohydrolase (NTPDase), 5'-nucleotidase, and adenosine deaminase (ADA), is capable of modulating the cerebral immune and inflammatory responses in silver catfish that is experimentally infected with Streptococcus agalactiae. Cerebral NTPDase (with ATP as substrate) and 5'-nucleotidase activities increased, while ADA activity decreased in silver catfish that is experimentally infected with S. agalactiae, compared to the control group. Moreover, the cerebral levels of ATP and Ado increased in infected animals compared to the uninfected control group. Brain histopathology in infected animals revealed inflammatory demyelination (the presence of occasional bubbly collections), increased cellular density in the area near to pia-mater and intercellular edema. Based on this evidence, the modulation of the purinergic cascade by the enzymes NTPDase, 5'-nucleotidase, and ADA exerts an anti-inflammatory profile due to the regulation of ATP and Ado levels. This suggests involvement of purinergic enzymes on streptococcosis pathogenesis, through regulating cerebral ATP and Ado levels, molecules known to participate in physiological or pathological events as inflammatory and anti-inflammatory mediators, respectively. In summary, the modulation of the cerebral purinergic cascade exerts an anti-inflammatory profile in an attempt to reduce inflammatory damage.


Assuntos
Encéfalo , Doenças dos Peixes , Proteínas de Peixes/imunologia , Peixes , Infecções Estreptocócicas , Streptococcus agalactiae/imunologia , Animais , Encéfalo/imunologia , Encéfalo/microbiologia , Doenças dos Peixes/imunologia , Doenças dos Peixes/microbiologia , Doenças dos Peixes/patologia , Peixes/imunologia , Peixes/microbiologia , Infecções Estreptocócicas/imunologia , Infecções Estreptocócicas/microbiologia , Infecções Estreptocócicas/veterinária
7.
Microb Pathog ; 111: 28-32, 2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-28807772

RESUMO

It is becoming evident that bacterial infectious diseases affect brain energy metabolism, where alterations of enzymatic complexes of the mitochondrial respiratory chain and creatine kinase (CK) lead to an impairment of cerebral bioenergetics which contribute to disease pathogenesis in the central nervous system (CNS). Based on this evidence, the aim of this study was to evaluate whether alterations in the activity of complex IV of the respiratory chain and CK contribute to impairment of cerebral bioenergetics during Streptococcus agalactiae infection in silver catfish (Rhamdia quelen). The activity of complex IV of the respiratory chain in brain increased, while the CK activity decreased in infected animals compared to uninfected animals. Brain histopathology revealed inflammatory demyelination, gliosis of the brain and intercellular edema in infected animals. Based on this evidence, S. agalactiae infection causes an impairment in cerebral bioenergetics through the augmentation of complex IV activity, which may be considered an adaptive response to maintain proper functioning of the electron respiratory chain, as well as to ensure ongoing electron flow through the electron transport chain. Moreover, inhibition of cerebral CK activity contributes to lower availability of ATP, contributing to impairment of cerebral energy homeostasis. In summary, these alterations contribute to disease pathogenesis linked to the CNS.


Assuntos
Encéfalo/metabolismo , Creatina Quinase Mitocondrial/metabolismo , Complexo IV da Cadeia de Transporte de Elétrons/metabolismo , Transporte de Elétrons/fisiologia , Metabolismo Energético , Infecções Estreptocócicas/metabolismo , Streptococcus agalactiae/patogenicidade , Trifosfato de Adenosina/metabolismo , Animais , Encéfalo/microbiologia , Encéfalo/patologia , Brasil , Peixes-Gato/microbiologia , Sistema Nervoso Central/metabolismo , Sistema Nervoso Central/microbiologia , Sistema Nervoso Central/patologia , Creatina Quinase/metabolismo , Doenças Desmielinizantes , Modelos Animais de Doenças , Doenças dos Peixes/enzimologia , Doenças dos Peixes/microbiologia , Doenças dos Peixes/patologia , Gliose/patologia , Homeostase , Humanos , Neutrófilos/microbiologia , Neutrófilos/patologia , Infecções Estreptocócicas/microbiologia
8.
Microb Pathog ; 111: 1-5, 2017 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-28804017

RESUMO

Xanthine oxidase (XO) is a final enzyme of purine metabolism linked with initiation and progression of infectious diseases, since is considered an important source of reactive oxygen species (ROS) and nitric oxide (NO), developing a pro-oxidant and pro-inflammatory profile in some infectious diseases. Thus, the aim of this study was to evaluate the involvement of XO activity in the renal oxidative and inflammatory damage, as well as the interplay with ROS and metabolites of nitric oxide (NOx) levels in silver catfish experimentally infected with Streptococcus agalactiae. Xanthine oxidase activity, and uric acid, ROS and NOx levels increased in renal tissue of infected animals compared to uninfected animals. Moreover, the histopathological analyses revealed the presence of necrosis, generalized edema and nuclear degeneration of renal tubules. Based on these evidences, the upregulation on renal XO activity exerts a pro-oxidant and pro-inflammatory profile in kidney of fish infected with S. agalactiae. The excessive uric acid levels induced the release of oxidative and inflammatory mediators, such as ROS and NOx, that directly contribute to renal oxidative and inflammatory damage. In summary, the upregulation on XO activity may be considered a pathway involved in the renal injury during S. agalactiae infection.


Assuntos
Rim/enzimologia , Óxido Nítrico/metabolismo , Oxirredução , Espécies Reativas de Oxigênio/metabolismo , Infecções Estreptocócicas/veterinária , Streptococcus agalactiae/patogenicidade , Xantina Oxidase/metabolismo , Animais , Brasil , Peixes-Gato , Modelos Animais de Doenças , Pesqueiros , Água Doce/química , Rim/lesões , Rim/microbiologia , Rim/patologia , Túbulos Renais/lesões , Estresse Oxidativo , Purinas/metabolismo , Infecções Estreptocócicas/patologia , Ácido Úrico/metabolismo
9.
Microb Pathog ; 110: 439-443, 2017 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-28735082

RESUMO

Cytosolic and mitochondrial creatine kinases (CK), through the creatine kinase-phosphocreatine (CK/PCr) system, provide a temporal and spatial energy buffer to maintain cellular energy homeostasis. However, the effects of bacterial infections on the kidney remain poorly understood and are limited only to histopathological analyses. Thus, the aim of this study was to investigate the involvement of cytosolic and mitochondrial CK activities in renal energetic homeostasis in silver catfish experimentally infected with Aeromonas caviae. Cytosolic CK activity decreased in infected animals, while mitochondrial CK activity increased compared to uninfected animals. Moreover, the activity of the sodium-potassium pump (Na+, K+-ATPase) decreased in infected animals compared to uninfected animals. Based on this evidence, it can be concluded that the inhibition of cytosolic CK activity by A. caviae causes an impairment on renal energy homeostasis through the depletion of adenosine triphosphate (ATP) levels. This contributes to the inhibition of Na+, K+-ATPase activity, although the mitochondrial CK activity acted in an attempt to restore the cytosolic ATP levels through a feedback mechanism. In summary, A. caviae infection causes a severe energetic imbalance in infected silver catfish, which may contribute to disease pathogenesis.


Assuntos
Aeromonas caviae/patogenicidade , Peixes-Gato/microbiologia , Creatina Quinase Mitocondrial/metabolismo , Citosol/metabolismo , Metabolismo Energético/fisiologia , Doenças dos Peixes/microbiologia , Infecções por Bactérias Gram-Negativas/veterinária , Rim/metabolismo , Adenosina Trifosfatases/metabolismo , Trifosfato de Adenosina/metabolismo , Animais , Brasil , Creatina Quinase/metabolismo , Citosol/enzimologia , Modelos Animais de Doenças , Doenças dos Peixes/patologia , Infecções por Bactérias Gram-Negativas/microbiologia , Infecções por Bactérias Gram-Negativas/patologia , Homeostase , Rim/microbiologia , Rim/patologia , Mitocôndrias/enzimologia , Mitocôndrias/metabolismo , Fosfocreatina/metabolismo , Fosforilação , ATPase Trocadora de Sódio-Potássio/metabolismo
10.
Microb Pathog ; 107: 349-353, 2017 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-28414167

RESUMO

It has long been recognized that there are several infectious diseases linked to the impairment of enzymatic complexes of the mitochondrial respiratory chain, with consequent production of reactive oxygen species (ROS), that contribute to disease pathogenesis. In this study, we determined whether the inhibition on mitochondrial respiratory chain might be considered a pathway involved in the production of ROS in gills of Rhamdia quelen experimentally infected by P. aeruginosa. The animals were divided into two groups with six fish each: uninfected (the negative control group) and infected (the positive control group). On day 7 post-infection (PI), animals were euthanized and the gills were collected to assess the activities of complexes I-III, II and IV of the respiratory chain, as well as ROS levels. The activities of complexes I-III, II and IV of the respiratory chain in gills decreased, while the ROS levels increased in infected compared to uninfected animals. Moreover, a significant negative correlation was found between enzymatic activity of the complexes I-III and IV related to ROS levels in P. aeruginosa infected animals, corroborating to our hypothesis that inhibition on complexes of respiratory chain leads to ROS formation. Also, microscopic severe gill damage and destruction of primary and secondary lamellae were observed in infected animals, with the presence of hyperplasia, leukocytic infiltration and telangiectasia. In summary, we have demonstrated, for the first time, that experimental infection by P. aeruginosa inhibits the activities of mitochondrial complexes of respiratory chain and, consequently, impairs the cellular energy homeostasis. Moreover, the inhibition on mitochondrial complexes I-III and IV are linked to the ROS production, contributing to disease pathogenesis.


Assuntos
Peixes-Gato/metabolismo , Transporte de Elétrons/efeitos dos fármacos , Doenças dos Peixes/microbiologia , Brânquias/metabolismo , Mitocôndrias/metabolismo , Pseudomonas aeruginosa/patogenicidade , Espécies Reativas de Oxigênio/antagonistas & inibidores , Animais , Citocromo-c Peroxidase , Modelos Animais de Doenças , Complexo I de Transporte de Elétrons/efeitos dos fármacos , Complexo IV da Cadeia de Transporte de Elétrons/efeitos dos fármacos , Doenças dos Peixes/patologia , Brânquias/enzimologia , Brânquias/patologia , Mitocôndrias/efeitos dos fármacos , Quinona Redutases , Espécies Reativas de Oxigênio/metabolismo
11.
Vet Microbiol ; 201: 121-125, 2017 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-28284597

RESUMO

Integration of mitochondria with cytosolic ATP-consuming/ATP-sensing and substrate supply processes is critical for gills bioenergetics, since this tissue plays an important role in the respiratory energy metabolism. The effects of bacterial infection on gills remain poorly understood, limited only to histopathological analyses. Thus, the aim of this study was to investigate whether experimental infection by Pseudomonas aeruginosa strain PA01 alters the enzymes of the phosphoryltransfer network (adenylate kinase (AK), pyruvate kinase (PK) and cytosolic and mitochondrial creatine kinase (CK)) in gills of silver catfish (Rhamdia quelen). The animals were divided into two groups with six fish each: uninfected (negative control) and infected (positive control). On day 7 post-infection (PI), animals were euthanized and the gills collected. AK, PK, and cytosolic and mitochondrial CK activities in gills decreased in infected compared to uninfected animals. Also, severe gill damage and destruction in the primary and secondary lamellae was observed in the infected animals. Therefore, we have demonstrated, for the first time, that experimental infection by P. aeruginosa inhibits key enzymes linked to the production and utilization of metabolic energy in silver catfish, and consequently, impairs cellular energy homeostasis, which may contribute to disease pathogenesis.


Assuntos
Adenilato Quinase/metabolismo , Peixes-Gato/metabolismo , Creatina Quinase/metabolismo , Metabolismo Energético , Doenças dos Peixes/microbiologia , Pseudomonas aeruginosa/fisiologia , Piruvato Quinase/metabolismo , Animais , Doenças dos Peixes/patologia , Brânquias/enzimologia , Brânquias/patologia , Homeostase
12.
Naunyn Schmiedebergs Arch Pharmacol ; 390(2): 139-148, 2017 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-27807596

RESUMO

The aim of this study was to investigate the effect of nerolidol-loaded nanospheres (N-NS) on the treatment of memory impairment caused by Trypanosoma evansi in mice, as well as oxidative stress, and Na+, K+-ATPase and acetylcholinesterase (AChE) activities in brain tissue. Animals were submitted to behavioral tasks (inhibitory avoidance task and open-field test) 4 days postinfection (PI). Reactive oxygen species (ROS) and thiobarbituric acid-reactive substance (TBARS) levels and catalase (CAT), superoxide dismutase (SOD), Na+, K+-ATPase and AChE activities were measured on the fifth-day PI. T. evansi-infected mice showed memory deficit, increased ROS and TBARS levels and SOD and AChE activities, and decreased CAT and Na+, K+-ATPase activities compared to uninfected mice. N-NS prevented memory impairment and oxidative stress parameters (except SOD activity), while free nerolidol (N-F) restored only CAT activity. Also, N-NS treatment was able to prevent alterations in Na+, K+-ATPase and AChE activities caused by T. evansi infection. A significantly negative correlation was observed between memory and ROS production (p < 0.001; r = -0.941), as well as between memory and AChE activity (p < 0.05; r = -0.774). On the contrary, a significantly positive correlation between memory and Na+, K+-ATPase activity was observed (p < 0.01; r = 0.844). In conclusion, N-NS was able to reverse memory impairment and to prevent increased ROS and TBARS levels due to amelioration of Na+, K+-ATPase and AChE activities and to activation of the antioxidant enzymes, respectively. These results suggest that N-NS treatment may be a useful strategy to treat memory dysfunction and oxidative stress caused by T. evansi infection.


Assuntos
Antioxidantes/administração & dosagem , Comportamento Animal/efeitos dos fármacos , Encéfalo/efeitos dos fármacos , Infecções Protozoárias do Sistema Nervoso Central/tratamento farmacológico , Inibidores da Colinesterase/administração & dosagem , Nanosferas , Estresse Oxidativo/efeitos dos fármacos , Sesquiterpenos/administração & dosagem , ATPase Trocadora de Sódio-Potássio/antagonistas & inibidores , Trypanosoma/patogenicidade , Tripanossomíase/tratamento farmacológico , Acetilcolinesterase/metabolismo , Animais , Aprendizagem da Esquiva/efeitos dos fármacos , Encéfalo/enzimologia , Encéfalo/patologia , Catalase/metabolismo , Infecções Protozoárias do Sistema Nervoso Central/enzimologia , Infecções Protozoárias do Sistema Nervoso Central/parasitologia , Infecções Protozoárias do Sistema Nervoso Central/psicologia , Transtornos Cognitivos/tratamento farmacológico , Transtornos Cognitivos/enzimologia , Transtornos Cognitivos/parasitologia , Transtornos Cognitivos/psicologia , Modelos Animais de Doenças , Feminino , Proteínas Ligadas por GPI/antagonistas & inibidores , Proteínas Ligadas por GPI/metabolismo , Memória/efeitos dos fármacos , Transtornos da Memória/tratamento farmacológico , Transtornos da Memória/enzimologia , Transtornos da Memória/parasitologia , Transtornos da Memória/psicologia , Camundongos , Atividade Motora/efeitos dos fármacos , Nootrópicos/administração & dosagem , Tempo de Reação/efeitos dos fármacos , Espécies Reativas de Oxigênio/metabolismo , ATPase Trocadora de Sódio-Potássio/metabolismo , Superóxido Dismutase/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Tripanossomíase/enzimologia , Tripanossomíase/parasitologia , Tripanossomíase/psicologia
13.
Parasitology ; 144(2): 148-157, 2017 02.
Artigo em Inglês | MEDLINE | ID: mdl-27748203

RESUMO

The aim of this study was to evaluate the effect of nerolidol free (N-F) and nerolidol-loaded in nanospheres (N-NS) on the hepatic antioxidant/oxidant status of mice experimentally infected by Trypanosoma evansi. In the liver it was measured: reactive oxygen species (ROS), thiobarbituric reactive acid substances (TBARS) and non-protein thiols (NPSH), catalase (CAT), superoxide dismutase (SOD) and glutathione-S-transferase (GST) and performed histopathological examination. In addition, seric levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. Liver samples from mice infected by T. evansi showed increased (P < 0·05) ROS, TBARS, AST and ALT levels and SOD activity, and decreased NPSH levels and CAT activity (P < 0·05) compared with uninfected animals. N-NS treatment prevented (P < 0·05) ROS and TBARS increase, and increased NPSH levels, and ameliorate CAT and SOD activities on liver of infected mice. Moreover, N-NS treatment reduced (P < 0·05) AST and ALT levels, and prevented histopathological changes caused by the parasite. N-NS protected the liver from the oxidative stress caused by T. evansi, which might be due to its antioxidant properties. Nerolidol might be considered a promising therapeutic agent against oxidative stress, and nanotechnology is an encouraging approach to be explored.


Assuntos
Fígado/patologia , Nanosferas/administração & dosagem , Estresse Oxidativo/efeitos dos fármacos , Sesquiterpenos/uso terapêutico , Tripanossomicidas/uso terapêutico , Trypanosoma/classificação , Tripanossomíase/tratamento farmacológico , Animais , Feminino , Fígado/parasitologia , Camundongos , Sesquiterpenos/administração & dosagem , Tripanossomicidas/administração & dosagem
14.
Clin Oral Implants Res ; 27(1): 31-8, 2016 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-25382721

RESUMO

AIM: The aim of this study is to evaluate the characteristics of socket repair after teeth extraction with loss of a bone plate. MATERIAL AND METHOD: Lower incisors were extracted from 120-day-old male rabbits. A standardized defect of 5 mm in the buccal plate was created in one of the socket sites. Furthermore, complete closures of the sockets entrance were performed. Two groups of biopsies were obtained: one with 14 days of healing and the other with 112, to perform the micro-CT and histological evaluations of the tested group with plate loss comparing with the control group with the intact buccal bone wall. RESULTS: Plate loss sites demonstrated reduction in width when compared to the intact ones and, this difference decreased with time. CONCLUSION: Long-term analysis showed that plate loss interfered in final ridge measurements by reducing the middle portion of the socket width compared to the intact plate sockets. The histological and micro-CT qualitative analysis showed that both sites presented similar pattern of healing, despite the reduced dimension found in plate loss sites.


Assuntos
Perda do Osso Alveolar/diagnóstico por imagem , Alvéolo Dental/diagnóstico por imagem , Alvéolo Dental/cirurgia , Microtomografia por Raio-X , Animais , Incisivo , Masculino , Coelhos , Fatores de Risco , Extração Dentária
15.
J Nanosci Nanotechnol ; 15(1): 800-9, 2015 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-26328444

RESUMO

In previous works, we developed nanocapsules and nanoemulsions containing the tea tree oil. The aim of this work was to prepare and characterize hydrogels containing these nanocarriers, and to evaluate their in vivo efficacy in protecting skin damage induced by UVB and cutaneous wound healing. Hydrogels were prepared using Carbopol Ultrez and their physicochemical characteristics were evaluated: macroscopic analysis, pH, spreadability and rheological properties. The in vivo antiedematogenic effect was evaluated by ear thickness measurement after UVB-irradiation. In order to evaluate healing action of hydrogels, we investigated the regression of the cutaneous lesion in rats. Hydrogels showed homogeneous aspect and pH values between 5.6-5.8 and a non-Newtonian behavior. The presence of nanocapsules and nanoemulsions in hydrogels did not change their spreadability profile. The inclusion of tea tree oil in the nanocapsules and nanoemulsions allowed reducing the edema induced by UVB exposure. Hydrogel containing nanocapsules presented a higher reduction of the wound area compared to the hydrogel containing nanoemulsions and hydrogel containing allantoin. This study shows the feasibility of obtained dermatological formulations containing the tea tree oil associated in nanostructured systems. These formulations represent a promising approach to topical treatment of inflammatory disorders and wound healing.


Assuntos
Hidrogéis/farmacologia , Nanocápsulas/química , Substâncias Protetoras/farmacologia , Pele/efeitos dos fármacos , Óleo de Melaleuca/farmacologia , Cicatrização/efeitos dos fármacos , Animais , Anti-Inflamatórios , Edema , Hidrogéis/química , Masculino , Substâncias Protetoras/química , Ratos , Ratos Wistar , Pele/lesões , Pele/fisiopatologia , Óleo de Melaleuca/química
16.
Mol Cell Biochem ; 403(1-2): 243-53, 2015 May.
Artigo em Inglês | MEDLINE | ID: mdl-25702177

RESUMO

Hypercholesterolemia and oxidative stress have been implicated in the pathophysiology of atherosclerosis and coronary artery disease. We investigated whether the carotenoid bixin (BIX) may reduce oxidative damage, inflammatory response, and the atherosclerotic lesion induced by hypercholesterolemia in rabbits. Rabbits received regular chow (control) or a hypercholesterolemic diet (0.5% cholesterol) alone or supplemented with BIX (10, 30 or 100 mg/kg body weight, b.w.) or simvastatin (15 mg/kg b.w.) for 60 days. Treatment with BIX or simvastatin reduced the atherosclerotic lesions in cholesterol-fed rabbits (up to 55 and 96% reduction, respectively). This protective effect of BIX was accompanied by decrease in the levels of tumor necrosis factor alpha by 15%, interleukin 6 by 19%, lipid peroxidation by 60%, non-high-density lipoprotein cholesterol (non-HDL-C) by 37%, and triglycerides by 41%. BIX increased by 160% the HDL-C levels and decreased by 67% the atherogenic index of hypercholesterolemic rabbits. In atherosclerotic rabbits, the non-protein thiol groups content and the activity of the antioxidant enzymes superoxide dismutase, catalase, glutathione reductase, and thioredoxin reductase were increased in the aortic tissue, whereas paraoxonase activity was reduced in the serum. All these changes were completely prevented by BIX or simvastatin treatment. These results demonstrate that BIX reduces the extent of atherosclerotic lesions and this effect was associated with the decrease in oxidative stress, inflammatory response, and improvement of dyslipidemia, which were most effectively controlled after treatment with 10-30 mg BIX/kg b.w. BIX consumption may, therefore, be an adjuvant to prevent atherosclerosis reducing risk factors for coronary diseases.


Assuntos
Anti-Inflamatórios/uso terapêutico , Antioxidantes/uso terapêutico , Aterosclerose/tratamento farmacológico , Carotenoides/uso terapêutico , Hipercolesterolemia/tratamento farmacológico , Lipídeos/sangue , Animais , Anti-Inflamatórios/farmacologia , Antioxidantes/farmacologia , Aorta/efeitos dos fármacos , Aorta/enzimologia , Aorta/patologia , Aterosclerose/sangue , Aterosclerose/complicações , Peso Corporal/efeitos dos fármacos , Carotenoides/química , Carotenoides/farmacologia , Hipercolesterolemia/sangue , Hipercolesterolemia/complicações , Masculino , Oxirredução/efeitos dos fármacos , Placa Aterosclerótica/sangue , Placa Aterosclerótica/patologia , Coelhos , Sinvastatina/farmacologia , Compostos de Sulfidrila/metabolismo , Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo , Fator de Necrose Tumoral alfa/sangue , Túnica Íntima/efeitos dos fármacos , Túnica Íntima/patologia
17.
Parasitology ; 140(5): 663-71, 2013 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-23361035

RESUMO

The aim of this study was to evaluate the anti-trypanosomal effect of treatment with 3'-deoxyadenosine (cordycepin) combined with deoxycoformycin (pentostatin: inhibitor of the enzyme adenosine deaminase) in vitro by using mice experimentally infected with Trypanosoma evansi. In vitro, a dose-dependent trypanocidal effect of cordycepin was observed against the parasite. In the in vivo trials, the two drugs were used individually and in combination of different doses. The drugs when used individually had no curative effect on infected mice. However, the combination of cordycepin (2 mg kg-1) and pentostatin (2 mg kg-1) was 100% effective in the T. evansi-infected groups. There was an increase in levels of some biochemical parameters, especially on liver enzymes, which were accompanied by histological lesions in the liver and kidneys. Based on these results we conclude that treatment using the combination of 3'-deoxyadenosine with deoxycoformycin has a curative effect on mice infected with T. evansi. However, the therapeutic protocol tested led to liver and kidney damage, manifested by hepatotoxicity and nephrotoxicity.


Assuntos
Desoxiadenosinas/uso terapêutico , Pentostatina/uso terapêutico , Tripanossomicidas/uso terapêutico , Trypanosoma/classificação , Tripanossomíase/tratamento farmacológico , Animais , Desoxiadenosinas/administração & dosagem , Relação Dose-Resposta a Droga , Quimioterapia Combinada/veterinária , Feminino , Camundongos , Pentostatina/administração & dosagem , Reação em Cadeia da Polimerase , Tripanossomicidas/administração & dosagem , Trypanosoma/efeitos dos fármacos
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