Poster
# 20
Poster |
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6th Internet World Congress for Biomedical Sciences |
María Dolores Mayas-Torres(1), José Manuel Martínez-Martos(2), María Jesús Ramírez-Expósito(3), María Jesús García-López(4), Isabel Prieto-Gómez(5), Garbiñe Arechaga-Maza(6), Manuel Ramírez-Sánchez(7)
(1)(2)(4)(5)(6)(7)Unit of Physiology. University of Jaén - Jaén. Spain
(3)Unit of Physiology. University of Jaen - Jaén. Spain
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[Endocrinology] |
[Neuroscience] |
[Pharmacology] |
[Physiology] |
[Toxicology] |
The present work shows that ethanol administration to frontal cortex mouse synaptosomes under our conditions (ethanol 25 mM, 50 mM and 100 mM during an incubation period of 15 minutes at 37°C), produces little signs of neurodegenerative processes. Using luminol as enhancer of chemiluminescence, it is not detected modifications in the free radical generation, although lucigenin chemiluminiscence indicates small increases in the production of free radicals, and in an inversely-proportional manner. That is specially perceptible when ethanol is given simultaneously with depolarized stimulus of synaptosomes. These free radicals seem to be the consequence of the increase in the mitochondrial activity, which is demonstrated by using MTT, but have little ability to induce degeneration. This is demonstrated by the inability of generating lipid peroxidation of the membrane lipids (lower doses of ethanol seems to have protector functions on basal levels) or protein oxidation of synaptosomes.
On the other hand, ethanol produces an inhibition dose-dependent of the basal levels of AspAP and GluAP, being this inhibition stronger in GluAP. After depolarization with K+ 25 mM a decrease of the AspAP and GluAP activities is produced. But the stimulation of synaptosomes with K+ 25 mM in presence of ethanol induces an inhibition of the activity inversely-proportional to the ethanol concentration, getting values such as the resulting of the stimulation with K+ 25 mM in ausence of ethanol. Because of this, the presence of ethanol on the artificial CSF in basal conditions does not produce an increase of the pool of exitatory amino acids. Under stimulant conditions, the presence of ethanol in the artificial CSF lead to smaller levels of enzymatic activity than control values. It could be due to an impairment of the homoeostatic processes generated at these levels. The aminopeptidase A activity (AspAP and GluAP)(1,17) is important not only due to its participation on the free excitatory amino acids pool generation by the release of N-terminal aminoacids of peptides and polypeptides, but because one of its physiologycal substrates is angiotensin II(18,19,20,21). This molecule participates in the control of the blood pressure in the brain(22,23), due to the existence of a regional brain renin-angiotensin system24. The modifications induced by ethanol in AspAP and GluAP activities could modify the regulation of the brain blood pressure, and be responsible of the neurotoxic processes that are coupled to the chronic intake of ethanol.
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[Endocrinology] |
[Neuroscience] |
[Pharmacology] |
[Physiology] |
[Toxicology] |
