SULM – Schweizerische Union für Labormedizin | Union Suisse de Médecine de Laboratoire | Swiss Union of Laboratory Medicine

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R Pantović1 , P Draganić2 , V Eraković3 , B Blagović1 , Č Milin1 , A Simonić2

1Department of Chemistry and Biochemistry, Faculty of Medicine, University of Rijeka, Croatia, 2Department of Pharmacology, Faculty of Medicine, University of Rijeka, Croatia, 3PLIVA Research Institute Ltd., Zagreb, Croatia

Fatty acids are the components of membrane phospholipids, having an important role in maintaining the structure and functions of the cell membranes. A release of fatty acids is one of the first pathophysiological events that follows primary trauma to the spinal cord, independently of the type of injury.1 The aim of this study was to determine the influence of injury and ethanol, the common substance of abuse and usual component of vehicle solutions, on the level of spinal cord free fatty acids (FFAs) in rabbits with experimantal spinal cord injury (SCI).

The free fatty acids were separated from the total lipid extract by preparative thin-layer chromatography. The free fatty acids, in the form of the corresponding methyl esters, were identified by using gas chromatography. The quantification was done using the internal standard.

The levels of free palmitic (16:0), stearic (18:0) and arachidonic (20:4 n-6) acids were significantly higher in the vehicle treated group in comparison to only laminectomised group. The level of FFAs in rabbits with a spinal cord injury shows a statistically significant increase in free palmitic, stearic, oleic (18:1), arachidonic and docosahexaenoic acids (22:6 n-3). Vehicle administration induced in the injured animals a significant increase of palmitic, stearic and oleic acid, while it induced a significant decrease of docosahexaenoic acids.

Summary and Conclusion:
SCI caused the spinal cord FFAs accumulation. The administration of ethanol (vehicle) induced an increase of some spinal cord free fatty acids level. Ethanol-induced FFA liberation may lead to a greater free radical production, the increase of GPX activity, therefore, representing a compensatory mechanism.
1. Bazan N, Rodrigez de Turco E, Allan G. Mediators of injury in neurotrauma. Intracellular signal transduction and gene expression. J Neurotrauma 1995; 12: 791-814.


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