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  • 1
    Electronic Resource
    Electronic Resource
    Changes induced by aging and drug treatment on cerebral enzymatic antioxidant system (1988)
    Springer
    Neurochemical research 13 (1988), S. 467-478 
    Details
    ISSN: 1573-6903
    Keywords: Antioxidant enzymes ; aging ; peroxidation ; drug treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The age-related modifications of the participants to the cerebral enzymatic antioxidant system (superoxide dismutase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase) were evaluated in four brain regions from male Wistar rats aged 5, 10, 15, 20, 25, 30, and 35 months. Both the specific enzyme activity and the profile of any enzyme tested markedly differ with age according to the region examined: parieto-temporal cortex, caudate-putamen, substantia nigra and thalamus. This inhomogeneous age-related profile of enzyme activities could explain both the controversial data of literature and the different regional vulnerability of the brain tissue to damage with aging. In rats aged 10, 20, or 30 months, the chronic i.p. treatment for two months with papaverine or ergot alkaloids (dihydroergocristine, dihydroergocornine, dehydroergocriptine) suggests that the antioxidant enzyme activities may be influenced according to the agent utilized, the brain region tested, and the age of the animal. In any case, small differences in the drug structure support marked differences in the type and extent of the intervention on the antioxidant enzymatic system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01268883
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  • 2
    Electronic Resource
    Electronic Resource
    Age-dependent changes of nucleic acid labeling in different rat brain regions (1989)
    Springer
    Neurochemical research 14 (1989), S. 701-706 
    Details
    ISSN: 1573-6903
    Keywords: Aging ; DNA ; ribosomal RNA ; poly(A)+ RNA ; CDP-choline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of aging on in vivo DNA and RNA labeling and on RNA content in various brain regions of 4-, 12-, and 24-month-old rats were investigated. No difference in [methyl-14C]thymidine incorporation into DNA of cerebral cortex and cerebelllum during aging was observed. The ratio of RNA/DNA content significantly decreased from 4 to 24 months of age in cerebral cortex, cerebellum and striatum. RNA labeling decreased by 15% in cerebral cortex of 24-month-old animals while in the other brain areas examined (cerebellum, hippocampus, hypothalamus, brainstem, striatum) did not change during aging. In the cerebral cortex, the ratio of the specific radioactivity of microsomal RNA to that of nuclear RNA, determined by in vivo experiments, was not affected by the aging process. A significant decrease of total, poly(A)+ RNA and poly(A)- RNA content was observed in the same brain area of 24-month-old rats compared to 4-month-old ones. Moreover, densitometric and radioactivity patterns obtained by gel electrophoresis of labeled RNA after in vitro experiments (tissue slices of cerebral cortex) showed a different ribosomal RNA processing during aging. In vivo chronic treatment with CDP-choline was able to increase RNA labeling in corpus striatum of 24-month-old animals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00964882
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  • 3
    Electronic Resource
    Electronic Resource
    Modifications by chronic intermittent hypoxia and drug treatment on skeletal muscle metabolism (1995)
    Springer
    Neurochemical research 20 (1995), S. 143-150 
    Details
    ISSN: 1573-6903
    Keywords: Hypoxia-normoxia cycles ; intermittent hypoxia ; skeletal muscle metabolism ; drug treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The energy metabolism was evaluated in gastrocnemius muscle from 3-month-old rats subjected to either mild or severe 4-week intermittent normobaric hypoxia. Furthermore, 4-week treatment with CNS-acting drugs, namely, α-adrenergic (δ-yohimbine), vasodilator (papaverine, pinacidil), or oxygen-increasing (almitrine) agents was performed. The muscular concentration of the following metabolites was evaluated: glycogen, glucose, glucose 6-phosphate, pyruvate, lactate, lactateto-pyruvate ratio; citrate, α-ketoglutarate, succinate, malate; aspartate, glutamate, alanine; ammonia; ATP, ADP, AMP, creatine phosphate. Furthermore the Vmax of the following muscular enzymes was evaluated: hexokinase, phosphofructokinase, pyruvate kinase, lactate dehydrogenase; citrate synthase, malate dehydrogenase; total NADH cytochrome c reductase; cytochrome oxidase. The adaptation to chronic intermittent normobaric mild or severe hypoxia induced alterations of the components in the anaerobic glycolytic pathway [as supported by the increased activity of lactate dehydrogenase and/or hexokinase, resulting in the decreased glycolytic substrate concentration consistent with the increased lactate production and lactate-to-pyruvate ratio] and in the mitochondrial mechanism [as supported by the decreased activity of malate dehydrogenase and/or citrate synthase resulting in the decreased concentration of some key components in the tricarboxylic acid cycle]. The effect of the concomitant pharmacological treatment suggests that the action of CNS-acting drugs could be also related to their direct influence on the muscular biochemical mechanisms linked to energy transduction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00970538
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  • 4
    Electronic Resource
    Electronic Resource
    Changes of mitochondrial membrane proteins in rat cerebellum during aging (1988)
    Springer
    Neurochemical research 13 (1988), S. 859-865 
    Details
    ISSN: 1573-6903
    Keywords: Mitochondrial membranes ; proteins ; cerebellum ; aging
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Qualitative and quantitative changes of mitochondrial membrane proteind during aging were investigated. Free (non-synaptic) mitochondria were purified from rat cerebellum at different ages (4, 8, 12, 16, 20, and 24 months). Mitochondrial outer membrane (OM), inner membrane (IM) and matrix (MX) were separated and the proteins were extracted and analyzed by gel-electrophoresis. After staining, the gels were scanned densitometrically to quantify the proteins. No significant changes in the quantity of OM or MX protein subunits were observed, while serveral statistically significant quantitative changes in IM proteins with age were found. These age-dependent modifications of inner membrane mitochondrial proteins may play an important role in energy transduction, transport systems and regulatory enzymatic activities in mitochondria.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00970754
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  • 5
    Electronic Resource
    Electronic Resource
    Changes of mitochondrial cytochrome c oxidase and FoF1 ATP synthase subunits in rat cerebral cortex during aging (1995)
    Springer
    Neurochemical research 20 (1995), S. 1465-1470 
    Details
    ISSN: 1573-6903
    Keywords: Cytochrome c oxidase ; FoF1 ATP synthase ; aging
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The contents of subunits I, II/III, and IV of cytochrome c oxidase and of subunits α, β and γ of FoF1 ATP synthase in inner mitochondrial membrane proteins purified from cerebral cortex of rat at 2, 6, 12, 18, 24, and 26 months of age were analyzed by western blot. Age-related changes in the content of subunits, either of mitochondrial or nuclear origin, were observed. All the cytochrome c oxidase (COX) subunits examined showed an age-related increase from 2-month-old rats up to 24 months with a decrease at the oldest age (26 months). The same pattern of age-dependent changes was observed for γ ATP synthase, while the α and β subunits increased progressively up to 26 months.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00970595
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  • 6
    Electronic Resource
    Electronic Resource
    Synaptosomal non-mitochondrial ATPase activities and drug treatment (1993)
    Springer
    Neurochemical research 18 (1993), S. 719-726 
    Details
    ISSN: 1573-6903
    Keywords: Almitrine ; ATPases ; clonidine ; δ-yohimbine ; synaptosomes ; theniloxazine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Energy-using non-mitochondrial ATPases were assayed in rat cerebral cortex synaptosomes and synaptosomal subfractions, namely synaptosomal plasma membranes and synaptic vesicles. The following enzyme activities were evaluated: Na+, K+-ATPase; high- and low-affinity Ca2+-ATPase; basal Mg2+-ATPase; Ca2+, Mg2+-ATPase. The evaluations were performed after four week-treatment with saline [controls] or α-adrenergic agents (δ-yohimbine, clonidine), energymetabolism interfering compound (theniloxazine), and oxygen-partial pressure increasing agent (almitrine), in order to define the plasticity and the selective changes in individual ATPases. In rat cerebral cortex, the enzyme adaptation to four-week-treatment with δ-yohimbine or clonidine was characterized by increase in both high- and low-affinity Ca2+-ATPase activities. The action involves the enzyme form located in the synaptic plasma membranes. The enzyme adaptation to the subchronic treatments with theniloxazine or almitrine was characterized by increase in Na+, K+-ATPase or Mg2+-ATPase activities, respectively. The action involves the enzymatic forms located in the synaptic plasma membranes. Thus, the pharmacodynamic effects of the agents tested should also be related to the changes induced in the activity of some specific synaptosomal nonmitochondrial ATPases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00966787
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  • 7
    Electronic Resource
    Electronic Resource
    Parkinson-like disease by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity inMacaca Fascicularis: Synaptosomal metabolism and action of dihydroergocriptine (1994)
    Springer
    Neurochemical research 19 (1994), S. 229-236 
    Details
    ISSN: 1573-6903
    Keywords: Parkinson-like syndrome by MPTP ; enzymes ; synaptosomes ; energy metabolism ; dihydroergocriptine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The maximal rates (Vmax) of some enzyme activities related to synaptosomal energy metabolism were studied in different types of synaptosomes from cerebellar cortex ofMacaca Fascicularis (Cynomolgus monkey). Different synaptosomal populations, namely “large” and “small” synaptosomes, were isolated from the anterior lobule of the cerebellar cortex of monkeys treated p.o. with dihydroergocriptine at the dose of 12 mg/kg/day before and during the induction of a Parkinson's-like syndrome by MPTP administration (i.v., 0.3 mg/kg/day for 5 days). The enzymes were chosen according to their regulatory role and as markers of the following metabolic pathways: (a) glycolysis ((hexokinase, phosphofructokinase, lactate dehydrogenase), (b) Krebs' (TCA) cycle (citrate synthase, malate dehydrogenase), (c) amino acid, glutamate metabolism (glutamate dehydrogenase, glutamate-pyruvate- and glutamate-oxaloacetate-transaminases), (d) acetylcholine catabolism (acetylcholinesterase) and (e) ATPases, i.e. Na+−K+-ATPase, Mg2+-ATP synthetase, Mg2+-ATPase, Ca2+−Mg2+-ATPase and Ca2+-ATPase Low and High affinity for Ca2+. The MPTP administration modified the activities of citrate synthase, malate dehydrogenase, Na+−K+-ATPase, acetylcholinesterase and glutamate-oxaloacetate transaminase only on selected types of synaptosomes. Pharmacological treatment by dihydroergocriptine was able to recovery at the steady-state levels the activities of these enzymes, thus demonstrating a partial protective effect on these biochemical parameters.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00971569
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  • 8
    Electronic Resource
    Electronic Resource
    Action of L-Acetylcarnitine on Different Cerebral Mitochondrial Populations from Cerebral Cortex (1998)
    Springer
    Neurochemical research 23 (1998), S. 1485-1491 
    Details
    ISSN: 1573-6903
    Keywords: Cerebral cortex ; energy metabolism ; enzymes ; L-acetylcarnitine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The maximum rate (Vmax) of some mitochondrial enzymatic activities related to the energy transduction (citrate synthase, α-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, cytochrome oxidase) and amino acid metabolism (glutamate dehydrogenase, glutamate-pyruvate-transaminase, glutamate-oxaloacetate-transaminase) was evaluated in non-synaptic (free) and intra-synaptic mitochondria from rat brain cerebral cortex. Three types of mitochondria were isolated from rats subjected to i.p. treatment with L-acetylcarnitine at two different doses (30 and 60 mg·kg−1, 28 days, 5 days/week). In control (vehicle-treated) animals, enzyme activities are differently expressed in non-synaptic mitochondria respect to intra-synaptic “light” and “heavy” ones. In fact, α-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, glutamate-pyruvate-transaminase and glutamate-oxaloacetate-transaminase are lower, while citrate synthase, cytochrome oxidase and glutamate dehydrogenase are higher in intra-synaptic mitochondria than in non-synaptic ones. This confirms that in various types of brain mitochondria a different metabolic machinery exists, due to their location in vivo. Treatment with L-acetylcarnitine decreased citrate synthase and glutamate dehydrogenase activities, while increased cytochrome oxidase and α-ketoglutarate dehydrogenase activities only in intra-synaptic mitochondria. Therefore in vivo administration of L-acetylcarnitine mainly affects some specific enzyme activities, suggesting a specific molecular trigger mode of action and only of the intra-synaptic mitochondria, suggesting a specific subcellular trigger site of action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020907400905
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  • 9
    Electronic Resource
    Electronic Resource
    Effect of In Vivo Administration of Naloxone on ATP-ase's Enzyme Systems of Synaptic Plasma Membranes from Rat Cerebral Cortex (2000)
    Springer
    Neurochemical research 25 (2000), S. 867-873 
    Details
    ISSN: 1573-6903
    Keywords: Cerebral cortex ; ATP-ases ; synaptic plasma membranes ; naloxone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Naloxone is a specific competitive antagonist of morphine, acting on opiate receptors, located on neuronal membranes. The effects of in vivo administration of naloxone on energy-consuming non-mitochondrial ATP-ases were studied in two different types of synaptic plasma membranes from rat cerebral cortex, known to contain a high density of opiate receptors. The enzyme activities of Na+, K+-ATP-ase, Ca2+, Mg2+-ATP-ase and Mg2+-ATP-ase and of acetylcholinesterase (AChE) were evaluated on synaptic plasma membranes obtained from control and treated animals with effective dose of naloxone (12μg · kg−1 i.m. 30 minutes). In control (vehicle-treated) animals specific enzyme activities assayed on these two types of synaptic plasma membranes are different, being higher on synaptic plasma membranes of II type than of I type, because the first fraction is more enriched in synaptic plasma membranes. The acute treatment with naloxone produced a significant decrease in Ca2+,Mg2+-ATP-ase activity and an increase in AChE activity, only in synaptic plasma membranes of II type. The decrease of Ca2+,Mg2+-ATP-ase enzymatic activity and the increased AChE activity are related to the interference of the drug on Ca2+ homeostasis in synaptosoplasm, that leads to the activation of calcium-dependent processes, i.e. the extrusion of neurotransmitter. These findings give further evidence that pharmacodynamic characteristics of naloxone are also related to increase [Ca2+] i , interfering with enzyme systems (Ca2+,Mg2+-ATP-ase) and that this drug increases acetylcholine catabolism in synaptic plasma membranes of cerebral cortex.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1007529826905
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  • 10
    Electronic Resource
    Electronic Resource
    Age-related effect induced by oxidative stress on the cerebral glutathione system (1989)
    Springer
    Neurochemical research 14 (1989), S. 473-481 
    Details
    ISSN: 1573-6903
    Keywords: Brain aging ; glutathione system ; free radicals ; oxidative stress ; ergot alkaloids ; papverine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the forebrain from male Wistar rats aged 5, 15 and 25 months, age-related putative alterations in the glutathione system (reduced and oxidized glutathione; redox index) were chronically induced by the administration in drinking water of free radical generators (hydrogen peroxide, ferrous chloride) or of inhibitors of endogenous free radical defenses (diethyl-dithio-carbamate, an inhibitor of superoxide dismutase activity). In hydrogen peroxide administered rats, both reduced glutathione and the cerebral glutathione redox index markedly declined as a function of aging, whereas oxidized glutathione consistently increased. In contrast, chronic iron intake failed to modify the reduced glutathione in forebrain from the rats of the different ages tested, whereas the oxidized glutathione was increased in the older brains. The chronic intake of diethyl-dithio-carbamate enhanced the concentrations of reduced glutathione in the forebrains from the rats of the different ages tested, the oxidized glutathione being unchanged. In 15-month-old rats submitted to chronic oxidative stress, ergot alkaloids (and particularly dihydroergocriptine) interfered with cerebral glutathione system, while papaverine was always ineffective. The comprehensive analysis of the data indicates that: (a) both the type of oxidative stress and the age of the animals modulate the cerebral responsiveness to the putative modifiers in the level of tissue free radicals; (b) aging magnifies the cerebral alterations induced by oxidative stress; the (c) cerebral glutathione system may be modified by metabolic rather than by circulatory interferences; (d) a balance between the various cerebral antioxidant defenses is present, the perturbation of an antioxidant system resulting in the compensatory modified activity of component(s) of another system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00964863
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