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

Contact address:

María Dolores Mayas-Torres Unit of Physiology University of Jaén Faculty of Experimental and Health Sciences Jaén E-23071 Spain jmmartos@ujaen.es

	[Endocrinology]	[Neuroscience]	[Pharmacology]	[Physiology]	[Toxicology]

ABSTRACT

Introduction. Investigations carried out in recent years indicate that one of the mechanisms responsible for neurodegenerative processes affecting the central nervous system is the hyperexcitabitily of amino acid neurotransmitters, particularly glutamic and aspartic acids. That excitatory amino acids act like strong endogenous toxins, which induce degeneration and neurone death. The activity of aminopeptidase A (AP-A) (GluAP and AspAP) releases glutamic and aspartic acids from biologically active peptides and polypeptides, regulating their activities. The purpose of this work was to study the role of AP-A as an index of neurotoxicity, using the toxic agent ethanol, under basal and stimulated conditions. Material and methods. The AP-A activity was determined in synaptosomes obtained from the frontal cortex of mouse using aspartate- and glutamate- -naphthylamide as substrates. The neurotoxic effects were analized by determinating the generation of free radicals, the lipid peroxidation of the membrane lipids and the oxidation of synaptosomal proteins. In addition, the bioenergetic behavior of synaptosomes was analized under the different experimental protocols. Results. Under basal conditions, AP-A activity is inhibited by ethanol, which depend on the concentration used, being the higher levels of inhibition levels observed for GluAP. Depolarization with K+ 25 mM induces an inhibition of AP-A. Ethanol, on stimulated conditions, induces a decrease of AP-A activity, but this inhibition dissapears when the ethanol concentration increase. On the other side, the presence of ethanol produces few signs of degeneration, although it enhances the energetic metabolism of synaptosomes. Conclusions. Alcohol leads to a decrease of AP-A activity under basal and stimulated conditions, although AspAP activity showed an inversely-proportional inhibition depending on the ethanol concentration. Under our experimental conditions, important signs of neurodegeneration are not observed. Therefore, the modifications of AP-A activity described may be related with degenerative processes that may occurs in a long term.

---

Keywords: Ethanol - Synaptosomes - Angiotensinase - Neurotoxicity - Excitatory amino acids -

---

Discussion Board

Any Comment to this presentation?

[ABSTRACT] [INTRODUCTION] [MATERIAL & METHODS] [RESULTS] [IMAGES] [DISCUSSION] [BIBLIOGRAPHY] [Discussion Board]

---

	[Endocrinology]	[Neuroscience]	[Pharmacology]	[Physiology]	[Toxicology]

María Dolores Mayas-Torres, José Manuel Martínez-Martos, María Jesús Ramírez-Expósito, María Jesús García-López, Isabel Prieto-Gómez, Garbiñe Arechaga-Maza, Manuel Ramírez-Sánchez
Copyright © 1999-2000. All rights reserved.

Last update: 15/01/00