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] |
Effects of ethanol on the bioenergetic behavior of synaptosomes.
The effects of ethanol on mitochondrial activity of mouse frontal cortex synaptosomes show the following results (table 1): Ethanol induces a dose-dependent increase of mitochondrial activity. In this way, ethanol 25 mM increases the activity in a 39.14% (p<0.01). Ethanol 50 mM produces a significant increase (p<0.01) in a 53.61% and ethanol 100 mM in a 58.92% (p<0.01).
Depolarization with K+ 25 mM induces an increase of mitochondrial activity in a 22.51% (p<0.01) (table 1). The simultaneous incubation of synaptosomes with K+ 25 mM and ethanol 25 mM or 50 mM increases significantly (p<0.01) the activity in a 36.52% and 46.43% respectively. Otherwise, ethanol 100 mM do not modify mitochondrial activity, when compared with the control values.
Parameters of oxidative stress.
The analysis of the ethanol effects on the free radical generation shows the following results: Ethanol 25 mM do not produce modifications in luminol chemiluminiscence when compared with control values. Ethanol 50 mM increases luminol chemiluminiscence in a 19.37% (p<0.05), while ethanol 100 mM induces a significant increase (p<0.05) of luminol chemiluminiscence in a 19.04% (table 1). Depolarization with K+ 25 mM does not modify luminol chemiluminiscence. In addition, the simultaneous incubation of synaptosomes with K+ 25 mM and ethanol does not change luminol chemiluminiscence either.
Using lucigenin as the enhancer of the chemiluminiscence signal, the results obtained are: Ethanol 25 mM induces a light increase of 18.05% (p<0.05), while ethanol 50 mM and 100 mM do not modify lucigenin chemiluminiscence, when compared with the control values (table 1). Depolarization with K+ 25 mM increases significantly (p<0.05) in a 16.94% lucigenin chemiluminiscence vs. the control values. However, the simultaneous incubation of synaptosomes with ethanol under depolarized conditions with K+ 25 mM 4), does not produce significant differences when compared with control values.
The effects of ethanol on lipid peroxidation (TBARS content) of mouse frontal cortex synaptosomes showed the following results: Ethanol 25 mM decreased TBARS content in a 13.55% (p<0.01) (table 1). Otherwise, ethanol 50 mM and 100 mM of ethanol did not modify significantly control values. Depolarization of synaptosomes with K+ 25 mM or the simultaneous incubation of synaptosomes with K+ 25 mM and ethanol at the different concentrations did not change TBARS content when compared with the control values (table 1).
Neither ethanol at the different concentrations used nor depolarization of synaptosomes with K+ 25 mM nor the simultaneous incubation of synaptosomes with K+ 25 mM and ethanol at different concentrations (25, 50, y 100 mM) did modify carbonyl content of synaptosomal proteins.
Effects of ethanol on AspAP activity.
The analysis of the effects of ethanol on the basal AspAP activity in mouse forntal cortex synaptosomes showed the following results: Ethanol inhibitis AspAP activity in a dose-dependent manner (figure 1A). Thus, ethanol 25 mM produces a significant inhibition (p<0.01) of 18.53% when compared with control values. Ethanol 50 mM decreases AspAP activity in a 38.55% (p<0.01), while ethanol 100 mM inhibitis in a 48.92% (p<0.01) (figure 1A).
After depolarization with K+ 25 mM, AspAP activity decreases in a 13.61% (p<0.01) (figure 1B). The simultaneous incubation of synaptosomes with K+ 25 mM and ethanol 25 mM produces a significant inhibition (p<0.01) of 52.68% when compared with control values (figure 1B). Ethanol 50 mM inhibits AspAP activity in a 15.59% (p<0.01). In presence of ethanol 100 mM, the depolarization with K+ 25 mM produces a significant decrease (p<0.05) of the AspAP levels in a 4.75% vs. the control values (figure 1B).
Effects of ethanol on GlluAP activity.
The analysis of the effects of ethanol on the basal GluAP activity in mouse frontal cortex synaptosomes shows the following results: Ethanol produces a dose-dependent inhibition of GluAP activity (figure 2A). In this way, ethanol 25 mM induces a significant inhibition (p<0.01) in a 49.09%. Ethanol 50 mM inhibits in a 54.27% (p<0.01), while ethanol 100 mM produces an inhibition of 65.3% (p<0.01) when compared with the control values (figure 2A).
The analysis of the effects of ethanol on GluAP activity after the stimulation of synaptosomes with K+ 25 mM shows the following results: Depolarization decreases significantly (p<0.01) GluAP activity in a 11.01% (figure 2B). The simultaneous incubation of synaptosomes with K+ 25 mM and ethanol 25 mM produces a significant inhibition (p<0.01) of GluAP activity in a 59.26% when compared with depolarized values (figure 2B). In addition, the presence of K+ 25 mM and ethanol 50 mM produces an inhibition of GluAP activity in a 55.99% (p<0.01) and ethanol 100 mM produces a significant decrease (p<0.01) of GluAP activity in a 26.86% vs. depolarized values (figure 2B).
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[Endocrinology] |
[Neuroscience] |
[Pharmacology] |
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[Toxicology] |
