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101.
The inhibitory effect of 23N-alkyl-4-piperidylesters (alkyl = ethyl-butyl) (APEA) and 8N-ethyl-2-pyrrolidinylmethylesters (EPMEA) of 2- and 3-substituted alkoxyphenylcarbamic acids (alkoxy = butoxy-heptyloxy-) on photosynthetic Hill reaction activity of spinach chloroplasts and on chlorophyll (Chl) synthesis in green algaeChlorella vulgaris was investigated. Inhibitory activities of these compounds were strongly connected with the lipophilicity of the whole molecule. A lower inhibitory activity of 2-alkoxy-substituted derivatives in relation to the corresponding 3-substituted ones was confirmed. Electron spin resonance (ESR) spectra of spinach chloroplasts demonstrated that the studied compounds affected the structure of photosystem (PS) 2 with the release of Mn2+ ions into interior of thylakoid membranes. 相似文献
102.
Zugno AI Stefanello FM Scherer EB Mattos C Pederzolli CD Andrade VM Wannmacher CM Wajner M Dutra-Filho CS Wyse AT 《Neurochemical research》2008,33(9):1804-1810
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) effects
of GAA on some oxidative stress parameters in rat striatum. Sixty-day-old rats were used for intrastriatal infusion of GAA.
For the in vitro studies, 60-day-old Wistar rats were killed by decapitation and the striatum was pre-incubated for 1 h at
37°C in the presence of GAA at final concentrations ranging from 10 to 100 μM. Parameters of oxidative stress such as total
radical-trapping antioxidant potential (TRAP), antioxidant enzymes (SOD, GPx, and CAT), protein carbonyl and thiol contents
were measured. DNA damage was also evaluated. Results showed that GAA administration (in vivo studies) or the addition of
100 μM GAA to assays (in vitro studies) significantly decreased TRAP, SOD activity, and total thiol levels in rat striatum.
In contrast, this guanidino compound did not alter protein carbonyl content and the activities of CAT and GPx. DNA damage was not found after intrastriatal administration of GAA. The data indicate that the metabolite accumulating in
GAMT deficiency decreases antioxidant capacity and total thiol content in the striatum. It is therefore presumed that this
pathomechanism may contribute at least in part to the pathophysiology of the brain injury observed in patients affected by
GAMT deficiency. 相似文献
103.
Pilla C Cardozo RF Dutra-Filho CS Wyse AT Wajner M Wannmacher CM 《Neurochemical research》2003,28(5):675-679
Maple syrup urine disease (MSUD) is an inherited metabolic disorder biochemically characterized by the accumulation of branched-chain amino acids (BCAAs) and their branched-chain keto acids (BCKAs) in blood and other tissues. Neurological dysfunction is usually present in the affected patients, but the mechanisms of brain damage in this disease are not fully understood. Considering that brain energy metabolism seems to be altered in MSUD, the main objective of this study was to investigate the in vitro effect of BCAAs and BCKAs on creatine kinase activity, a key enzyme of energy homeostasis, in brain cortex of young rats. BCAAs, but not their BCKAs, significantly inhibited creatine kinase activity at concentrations similar to those found in the plasma of MSUD patients (0.5–5 mM). Considering the crucial role creatine kinase plays in energy homeostasis in brain, if this effect also occurs in the brain of MSUD patients, it is possible that inhibition of this enzyme activity may contribute to the brain damage found in this disease. 相似文献
104.
The method of affinity coelectrophoresis was used to study the binding of
nine representative glycosaminoglycan (GAG)-binding proteins, all thought
to play roles in nervous system development, to GAGs and proteoglycans
isolated from developing rat brain. Binding to heparin and non-neural
heparan and chondroitin sulfates was also measured. All nine
proteins-laminin-1, fibronectin, thrombospondin-1, NCAM, L1, protease
nexin-1, urokinase plasminogen activator, thrombin, and fibroblast growth
factor-2-bound brain heparan sulfate less strongly than heparin, but the
degree of difference in affinity varied considerably. Protease nexin-1
bound brain heparan sulfate only 1.8- fold less tightly than heparin
(Kdvalues of 35 vs. 20 nM, respectively), whereas NCAM and L1 bound heparin
well (Kd approximately 140 nM) but failed to bind detectably to brain
heparan sulfate (Kd>3 microM). Four proteins bound brain chondroitin
sulfate, with affinities equal to or a few fold stronger than the same
proteins displayed toward cartilage chondroitin sulfate. Overall, the
highest affinities were observed with intact heparan sulfate proteoglycans:
laminin-1's affinities for the proteoglycans cerebroglycan (glypican-2),
glypican-1 and syndecan-3 were 300- to 1800-fold stronger than its affinity
for brain heparan sulfate. In contrast, the affinities of fibroblast growth
factor-2 for cerebroglycan and for brain heparan sulfate were similar.
Interestingly, partial proteolysis of cerebroglycan resulted in a >400-
fold loss of laminin affinity. These data support the views that (1)
GAG-binding proteins can be differentially sensitive to variations in GAG
structure, and (2) core proteins can have dramatic, ligand-specific
influences on protein-proteoglycan interactions.
相似文献
105.
Benvegnú Dalila Moter Roversi Katiane Barcelos Raquel Cristine Silva Trevizol Fabíola Pase Camila Simonetti Segat Hecson Jesser Dias Verônica Tironi Savian Ana Luiza Piccoli Bruna Lopes Piccolo Jaqueline Dutra-Filho Carlos Severo Emanuelli Tatiana de Bona da Silva Cristiane Beck Ruy Carlos Ruver Burger Marilise Escobar 《Neurochemical research》2018,43(2):477-487
Neurochemical Research - Haloperidol is a widely used antipsychotic, despite the severe motor side effects associated with its chronic use. This study was carried out to compare oral dyskinesia... 相似文献
106.
Rosa AP Jacques CE Moraes TB Wannmacher CM de Mattos Dutra A Dutra-Filho CS 《Cellular and molecular neurobiology》2012,32(7):1113-1118
Phenylketonuria is a recessive autosomal disorder that is caused by a deficiency in the activity of phenylalanine-4-hydroxylase, which converts phenylalanine to tyrosine, leading to the accumulation of phenylalanine and its metabolites phenyllactic acid, phenylacetic acid, and phenylpyruvic acid in the blood and tissues of patients. Phenylketonuria is characterized by severe neurological symptoms, but the mechanisms underlying brain damage have not been clarified. Recent studies have shown the involvement of oxidative stress in the neuropathology of hyperphenylalaninemia. Glucose-6-phosphate dehydrogenase plays an important role in antioxidant defense because it is the main source of reduced nicotinamide adenine dinucleotide phosphate (NADPH), providing a reducing power that is essential in protecting cells against oxidative stress. Therefore, the present study investigated the in vitro effect of phenylalanine (0.5, 1, 2.5, and 5?mM) and its metabolites phenyllactic acid, phenylacetic acid, and phenylpyruvic acid (0.2, 0.6, and 1.2?mM) on the activity of enzymes of the pentose phosphate pathway, which is involved in the oxidative phase in rat brain homogenates. 6-Phosphogluconate dehydrogenase activity was not altered by any of the substances tested. Phenylalanine, phenyllactic acid, and phenylacetic acid had no effect on glucose-6-phosphate dehydrogenase activity. Phenylpyruvic acid significantly reduced glucose-6-phosphate dehydrogenase activity without pre-incubation and after 1?h of pre-incubation with the homogenates. The inhibition of glucose-6-phosphate dehydrogenase activity caused by phenylpyruvic acid could elicit an impairment of NADPH production and might eventually alter the cellular redox status. The role of phenylpyruvic acid in the pathophysiological mechanisms of phenylketonuria remains unknown. 相似文献
107.
Ferreira AG da Cunha AA Machado FR Pederzolli CD Dalazen GR de Assis AM Lamers ML dos Santos MF Dutra-Filho CS Wyse AT 《Journal of cellular biochemistry》2012,113(1):174-183
The present study investigated the effects of chronic hyperprolinemia on oxidative and metabolic status in liver and serum of rats. Wistar rats received daily subcutaneous injections of proline from their 6th to 28th day of life. Twelve hours after the last injection the rats were sacrificed and liver and serum were collected. Results showed that hyperprolinemia induced a significant reduction in total antioxidant potential and thiobarbituric acid-reactive substances. The activities of the antioxidant enzymes catalase and superoxide dismutase were significantly increased after chronic proline administration, while glutathione (GSH) peroxidase activity, dichlorofluorescin oxidation, GSH, sulfhydryl, and carbonyl content remained unaltered. Histological analyses of the liver revealed that proline treatment induced changes of the hepatic microarchitecture and increased the number of inflammatory cells and the glycogen content. Biochemical determination also demonstrated an increase in glycogen concentration, as well as a higher synthesis of glycogen in liver of hyperprolinemic rats. Regarding to hepatic metabolism, it was observed an increase on glucose oxidation and a decrease on lipid synthesis from glucose. However, hepatic lipid content and serum glucose levels were not changed. Proline administration did not alter the aminotransferases activities and serum markers of hepatic injury. Our findings suggest that hyperprolinemia alters the liver homeostasis possibly by induction of a mild degree of oxidative stress and metabolic changes. The hepatic alterations caused by proline probably do not implicate in substantial hepatic tissue damage, but rather demonstrate a process of adaptation of this tissue to oxidative stress. However, the biological significance of these findings requires additional investigation. 相似文献
108.
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
109.
110.
Contrasting population structure from nuclear intron sequences and mtDNA of humpback whales 总被引:21,自引:4,他引:21
Powerful analyses of population structure require information from multiple
genetic loci. To help develop a molecular toolbox for obtaining this
information, we have designed universal oligonucleotide primers that span
conserved intron-exon junctions in a wide variety of animal phyla. We test
the utility of exon-primed, intron-crossing amplifications by analyzing the
variability of actin intron sequences from humpback, blue, and bowhead
whales and comparing the results with mitochondrial DNA (mtDNA) haplotype
data. Humpback actin introns fall into two major clades that exist in
different frequencies in different oceanic populations. It is surprising
that Hawaii and California populations, which are very distinct in mtDNAs,
are similar in actin intron alleles. This discrepancy between mtDNA and
nuclear DNA results may be due either to differences in genetic drift in
mitochondrial and nuclear genes or to preferential movement of males, which
do not transmit mtDNA to offspring, between separate breeding grounds.
Opposing mtDNA and nuclear DNA results can help clarify otherwise hidden
patterns of structure in natural populations.
相似文献