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  • 1
    Electronic Resource
    Electronic Resource
    Glutamic Acid and γ-Aminobutyric Acid Modulate Each Other's Release Through Heterocarriers Sited on the Axon Terminals of Rat Brain (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 61 (1993), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The effects of γ-aminobutyric acid (GABA) on the spontaneous release of endogenous glutamic acid (Glu) or aspartic acid (Asp) and the effects of Glu on the release of endogenous GABA or [3H]GABA were studied in superfused rat cerebral cortex synaptosomes. GABA increased the outflow of Glu (EC5017.2 μM) and Asp (EC50 18.4 μM). GABA was not antagonized by bicuculline or picrotoxin. Neither muscimol nor (-)-baclofen mimicked GABA. The effects of GABA were prevented by GABA uptake inhibitors and were Na+ dependent. Glu enhanced the release of [3H]GABA (EC50 11.5 μM) from cortical synaptosomes. Glu was not mimicked by the glutamate receptor agonists N-methyl-d-aspartic, kainic, or quisqualic acid. The Glu effect was decreased by the Glu uptake inhibitor D-threo-hydroxyaspartic acid (THA) and it was Na+ sensitive. Similarly to Glu, D-Asp increased [3H]GABA release (EC50 9.9 μM), an effect blocked by THA. Glu also increased the release of endogenous GABA from cortex synaptosomes. In this case the effect was in part blocked by the (RS)-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antagonist 6-cyano-7-nitroquinoxaiine-2, 3-dione, whereas the 6-cyano-7-nitroquinoxaline- 2, 3-dione-insensitive portion of the effect was prevented by THA. GABA increased the [3H]D-Asp outflow (EC50 13.7 μM) from hippocampal synaptosomes in a muscimol-, (-)- baclofen-, bicuculline-, and picrotoxin-insensitive manner. The GABA effect was abolished by blocking GABA uptake and was Na+ dependent. Glu increased the release of [3H]- GABA from hippocampal synaptosomes (EC50 7.1 μM) in an N-methyl-d-aspartic acid-, kainic acid-, or quisqualic acid-insensitive way. The effect of Glu was prevented by THA and was Na+ dependent. As in the cortex, the effect of Glu was mimicked by D-Asp in a THA-sensitive manner. It is proposed that high-affinity GABA or Glu heterocarriers are sited respectively on glutamatergic or GA- BAergic nerve terminals in rat cerebral cortex and hippocampus. The uptake of GABA may modulate Glu and Asp release, whereas the uptake of Glu may modulate the release of GABA. The existence of these heterocarriers is in keeping with the reported colocalization of GABA and Glu in some cortical and hippocampal neurons. Preliminary data suggest that these mechanisms may also be present in rat cerebellum and spinal cord.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1993.tb03558.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Protein and Lipid Oxidative Stresses During Cheese Manufacture (2001)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of food science 66 (2001), S. 0 
    Details
    ISSN: 1750-3841
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Process Engineering, Biotechnology, Nutrition Technology
    Notes: : The amounts of protein-bound carbonyls (PC), malondialdehyde, (MDA) and the tocopherolquinone/ tocopherol ratio (TQ) were used as markers to evaluate the oxidative damage during manufacture. Their concentrations were determined in 11 Italian cheese varieties produced with different curd heat treatments. A positive correlation between heat intensity and oxidative damage was found (p 〈 0.05). No correlation was seen between ripening time and oxidation extent in differently ripened Grana Padano cheese. Positive correlation between heating and TQ and PC levels was found (p 〈 0.001 and 0.05, respectively) in Grana Padano cheese produced with milk pasteurized at 58, 68, or 72 °C. Pasteurization ad curdling steps, during mozzarella cheesemaking, highly contributed to TQ yield.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2621.2001.tb08214.x
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  • 3
    Electronic Resource
    Electronic Resource
    In vivo activation of N-methyl-d-aspartate receptors in the rat hippocampus increases prostaglandin E2 extracellular levels and triggers lipid peroxidation through cyclooxygenase-mediated mechanisms (2002)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 81 (2002), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Cyclooxygenases (COX) are a family of enzymes involved in the biosynthesis of prostaglandin (PG) and thromboxanes. The inducible enzyme cyclooxygenase-2 (COX-2) is the major isoform found in normal brain, where it is constitutively expressed in neurons and is further up-regulated during several pathological events, including seizures and ischaemia. Emerging evidence suggests that COX-2 is implicated in excitotoxic neurodegenerative phenomena. It remains unclear whether PGs or other products associated to COX activity take part in these processes. Indeed, it has been suggested that reactive oxygen species, produced by COX, could mediate neuronal damage. In order to obtain direct evidence of free radical production during COX activity, we undertook an in vivo microdialysis study to monitor the levels of PGE2 and 8-epi-PGF2α following infusion of N-methyl-d-aspartate (NMDA). A 20-min application of 1 mm NMDA caused an immediate, MK-801-sensitive increase of both PGE2 and 8-epi-PGF2α basal levels. These effects were largely prevented by the specific cytosolic phospholipase A2 (cPLA2) inhibitor arachidonyl trifluoromethyl ketone (ATK), by non- selective COX inhibitors indomethacin and flurbiprofen or by the COX-2 selective inhibitor NS-398, suggesting that the NMDA-evoked prostaglandin synthesis and free radical-mediated lipid peroxidation are largely dependent on COX-2 activity. As several lines of evidence suggest that prostaglandins may be potentially neuroprotective, our findings support the hypothesis that free radicals, rather than prostaglandins, mediate the toxicity associated to COX-2 activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2002.00897.x
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Measurement by ELISA of Active Lectin in Dietary Supplements Containing Kidney Bean Protein (2003)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of food science 68 (2003), S. 0 
    Details
    ISSN: 1750-3841
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Process Engineering, Biotechnology, Nutrition Technology
    Notes: : We describe an ELISA assay to measure the active lectin content in dietary supplements containing protein extracts from Phaseolus vulgaris. Phytohemagglutinin (PHA) is known to induce serious consequences for metabolism and health when consumed raw or only lightly cooked. The ELISA was performed using plates preliminarily coated with porcine thyroglobulin, which has high specificity binding to active lectin. The bound active lectin was detected by a rabbit anti-PHA IgG and a secondary antibody enzyme conjugate. An assessment of linearity and analytical range were also performed. The data obtained showed good repeatability, specificity and a limit of quantification of 15 ng of PHA. The sensitivity of the method corresponds to 30 ppm.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2621.2003.tb09640.x
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    Paper (German National Licenses)
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