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Acta Physiologica 2009; Volume 195, Supplement 667
XXXV Congress of The Spanish Society for Physiological Sciences
2/17/2009-2/20/2009
Valencia, Spain
OXIDIZED SUNFLOWER OIL CONTAINING 4-HYDROPEROXY- AND 4-HYDROXY-TRANS-2-NONENAL ALTERS CORTICAL TRKA RECEPTOR EXPRESSION IN RATS
Abstract number: P66
Zarate1 J, Goicoechea1 E, Pascual1 J, Echevarria1 E, Guillen1 MD
1Department of Physiology, Department of Food Technology, Faculty of Pharmacy, University of the Basque Country, Vitoria, Spain
Sunflower oil in a specific oxidation stage (containing 4-hydroperoxy- and 4-hydroxy-trans-2-nonenal), reached at 70 °C with aeration, was administered intraperitoneally to rats. This oil, under these oxidative conditions, generates hydroperoxides, which accumulate up to reach a certain level, after which their sharp degradation is produced. The oil administered to the rats is just in the step in which this sharp degradation of primary oxidation compounds is produced leading to the formation of significant proportions of secondary oxidation products; among these latter, aldehydes constitute an important group. Sunflower oil oxidation, under the above mentioned conditions, has as characteristic that generates several oxygenated a,b unsaturated aldehydes, among which 4-hydroperoxy-trans-2-alkenals and 4-hydroxy-trans-2-alkenals are the main. An amount of 3 ml/kg/day for 21 days of oxidized sunflower oil was administered to Male Sprague-Dawley rats. The control group was administered non-oxidized sunflower oil in the same volume and duration as the experimental group. A significant decrease in the numbers of neural cells positively immunostained for TrkA receptor was detected in the frontal cortex of the experimental group, with respect to controls, suggesting neuronal damage, as well as a deficit in neuronal survival signalling at this level, that could lead to apoptosis of cholinergic neurons, which play a key role in memory and attention function. These results indicate that toxic substances present in the oxidized sunflower oil, among which are 4-hydroxy-trans-2-nonenal (HNE) and 4-hydroperoxy-trans-2-nonenal, could disrupt survival signallings of frontal cortex cholinergic neurons, which could lead to apoptosis and neurodegenerative diseases.
We would like to thank Juan Manuel Rodriguez Robledo for his technical assistance. This work has been partially supported by the Ministerio de Ciencia y Tecnología (MCYT, AGL2006-01381) and the Universidad del País Vasco (GIU05/25). E. Goicoechea thanks the Gobierno Vasco for a predoctoral fellowship/contract.
To cite this abstract, please use the following information:
Acta Physiologica 2009; Volume 195, Supplement 667 :P66