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161.
Zugno AI Oliveira DL Scherer EB Wajner M Wofchuk S Wyse AT 《Neurochemical research》2007,32(6):959-964
Glutamate plays a central role in the excitatory synaptic transmission and is important for brain development and functioning.
Increased glutamate levels in the synaptic cleft are related to neuronal damage associated with excitotoxicity. Guanidinoacetate
methyltransferase (GAMT) deficiency is an inherited neurometabolic disorder biochemically characterized by tissue accumulation
of guanidinoacetate (GAA) and depletion of creatine. Affected patients present epilepsy and mental retardation whose pathogeny
is unclear. In the present study we investigated the in vitro and in vivo (intrastriatal administration) effect of GAA on
glutamate uptake by striatum slices of developing and adult rats. Results showed that GAA significantly inhibited in vitro
glutamate uptake at 50 μM and 100 μM in all ages tested. We also tested the effect of taurine on the inhibition of glutamate
uptake caused by GAA. Taurine significantly attenuated the inhibitory effect caused by 50 μM GAA, but did not alter that provoked
by 100 μM GAA. Furthermore, intrastriatal administration of a solution of 30 μM GAA (0.06 nmol/striatum) significantly inhibited
glutamate uptake by rat striatum slices. Our results suggest that the inhibition of striatal glutamate uptake caused by GAA
might be involved in the neuropathology and especially in the acute neurological features present in patients with GAMT-deficiency. 相似文献
162.
163.
Latini A Ferreira GC Scussiato K Schuck PF Solano AF Dutra-Filho CS Vargas CR Wajner M 《Cellular and molecular neurobiology》2007,27(4):423-438
1. Glutaric acidemia type I (GA I) is a neurometabolic disorder caused by deficiency of glutaryl-CoA dehydrogenase, which
leads to tissue accumulation of predominantly glutaric acid (GA) and also 3-hydroxyglutaric acid to a lesser amount. Affected
patients usually present progressive cortical atrophy and acute striatal degeneration attributed to the toxic accumulating
metabolites.
2. In the present study, we determined a number of oxidative stress parameters, namely chemiluminescence, thiobarbituric acid-reactive
substances (TBA-RS), total antioxidant reactivity (TAR), glutathione (GSH) levels, and the activities of catalase and glutathione
peroxidase (GPx), in various tissues from rats chronically exposed to GA or to saline (controls). High GA concentrations,
similar to those found in glutaric aciduria type I, were induced in the brain by three daily subcutaneous injections of saline-buffered
GA (5 μmol/g body weight) to Wistar rats of 5–22 days of life. The parameters were assessed 12 h after the last GA administration
in different brain structures, skeletal muscle, heart, liver, erythrocytes, and plasma. The lipid peroxidation parameters
chemiluminescence and/or TBA-RS measurements were found significantly increased in midbrain, liver, and erythrocytes of GA-injected
rats. The activity of GPx was significantly reduced in midbrain and markedly increased in liver. TAR measurement was significantly
reduced in midbrain and liver. Furthermore, GSH levels were reduced in liver and heart.
We also investigated the acute in vivo effect of GA administration on the same oxidative stress parameters in cerebral structures and erythrocytes from 22-day-old
rats. We found that TBA-RS values were significantly increased in erythrocytes, TAR levels were markedly decreased in midbrain
and cerebellum, and GPx activity mildly reduced in the midbrain.
3. These data showing an imbalance between antioxidant defences and oxidative damage, particularly in midbrain, liver, and
erythrocytes from GA-injected rats, indicate that oxidative stress might be involved in GA toxicity and that the midbrain,
where the striatum is located, is the brain structure more susceptible to GA chronic and acute exposition. 相似文献
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165.
Maciel EN Kowaltowski AJ Schwalm FD Rodrigues JM Souza DO Vercesi AE Wajner M Castilho RF 《Journal of neurochemistry》2004,90(5):1025-1035
Changes in mitochondrial integrity, reactive oxygen species release and Ca2+ handling are proposed to be involved in the pathogenesis of many neurological disorders including methylmalonic acidaemia and Huntington's disease, which exhibit partial mitochondrial respiratory inhibition. In this report, we studied the mechanisms by which the respiratory chain complex II inhibitors malonate, methylmalonate and 3-nitropropionate affect rat brain mitochondrial function and neuronal survival. All three compounds, at concentrations which inhibit respiration by 50%, induced mitochondrial inner membrane permeabilization when in the presence of micromolar Ca2+ concentrations. ADP, cyclosporin A and catalase prevented or delayed this effect, indicating it is mediated by reactive oxygen species and mitochondrial permeability transition (PT). PT induced by malonate was also present in mitochondria isolated from liver and kidney, but required more significant respiratory inhibition. In brain, PT promoted by complex II inhibition was stimulated by increasing Ca2+ cycling and absent when mitochondria were pre-loaded with Ca2+ or when Ca2+ uptake was prevented. In addition to isolated mitochondria, we determined the effect of methylmalonate on cultured PC12 cells and freshly prepared rat brain slices. Methylmalonate promoted cell death in striatal slices and PC12 cells, in a manner attenuated by cyclosporin A and bongkrekate, and unrelated to impairment of energy metabolism. We propose that under conditions in which mitochondrial complex II is partially inhibited in the CNS, neuronal cell death involves the induction of PT. 相似文献
166.
Anderson L. Luiz Bruno Perlatti Fabiana A. Marques Edson Rodrigues-Filho Eduardo N. Costa Zulene A. Ribeiro Wellington I. Eduardo Arlindo L. Boiça-Júnior Maristela Imatomi Tadeusz Gorecki Moacir Rossi Forim 《Ecological Research》2017,32(3):435-444
Botanical extracts are a plentiful resource of molecules with different biological activities, such as insecticides and antimicrobial pesticides. In this context, the aim of this work was to evaluate the efficacy of botanical extracts from the Brazilian savannah against Diabrotica speciosa and bacterial strains isolated from the gut of this insect under aseptic conditions. The bacterial isolates were identified by genomic and proteomic approaches, and bioassayed against eighteen botanical extracts in vitro. The best results of bacterial inhibitions were obtained for the extracts of Casearia sylvestris and Psidium laruotteanum. Fractions of C. sylvestris and P. laruotteanum, quantitatively evaluated by chromatographic analyses, showed a relationship between the bactericidal activity and phytochemical profile. In vivo assays showed that P. laruotteanum was also effective for the control of D. speciosa. Those results show that selected natural products can have both antimicrobial and insecticidal activities. 相似文献
167.
Aline E. Casaril Carlos G. Santos Bruno S. Marangoni Sandro M. Lima Luis H. C. Andrade Wagner S. Fernandes Jucelei O. M. Infran Natália O. Alves Moacir D. G. L. Borges Cicero Cena Alessandra G. Oliveira 《Journal of biophotonics》2021,14(4):e202000412
Lutzomyia longipalpis and Lutzomyia cruzi are the main sandflies species involved in the transmission of Leishmania infantum protozoan in Brazil. The morphological characteristics can be used for species identification of males specimens, while females are indistinguishable. Although, sandflies identification is essential to understand vectorial capacity, and susceptibility to infectious agents or insecticides, there is a lack of new strategies for specimen identification. In this study, Fourier transform infrared photoacoustic spectroscopy combined with multivariate analysis identified intraspecific differences between Lutzomyia populations. Successfully group clustering was achieved by principal component analysis. The main differences observed can be related to the protein content of the specimens. A classification with 100% accuracy was obtained using machine learning approach, allowing the identification of sandflies specimens. 相似文献
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169.
Sustained levels of leucine comparable to those of human Maple Syrup Urine Disease (MSUD) were achieved in blood and brain of rats by subcutaneous leucine administration twice a day from the 6th to the 28th day of life. Control rats were treated with saline in the same volumes. Behavioral studies using aversive and nonaversive tasks were performed during adult age. Chronic early leucine treatment impaired acquisition of a two-way shuttle avoidance task and altered habituation to an open field. Our results suggest that early postnatal leucine administration induces long-lasting behavioral deficits. 相似文献
170.