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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Neurochemical research 14 (1989), S. 473-481 
    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
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Neurochemical research 18 (1993), S. 719-726 
    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
    Library Location Call Number Volume/Issue/Year Availability
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