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International Journal of Vascular Medicine
Volume 2012, Article ID 898769, 7 pages
Research Article

Lipofundin-Induced Hyperlipidemia Promotes Oxidative Stress and Atherosclerotic Lesions in New Zealand White Rabbits

1Center of Studies for Research and Biological Evaluations, Pharmacy and Food Science College, University of Havana, PO. Box 13 600, La Coronela, La Lisa, Havana 13600, Cuba
2Department of Antibody Engineering, Center of Molecular Immunology, Havana 11600, Cuba
3Department of Electron Microscopy, Center for Genetic Engineering and Biotechnology, Havana 10600, Cuba
4MediNat, 60021 Ancona, Italy

Received 1 April 2011; Revised 21 June 2011; Accepted 23 July 2011

Academic Editor: Spencer D. Proctor

Copyright © 2012 Livan Delgado Roche et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Atherosclerosis represents a major cause of death in the world. It is known that Lipofundin 20% induces atherosclerotic lesions in rabbits, but its effects on serum lipids behaviour and redox environment have not been addressed. In this study, New Zealand rabbits were treated with 2 mL/kg of Lipofundin for 8 days. Then, redox biomarkers and serum lipids were determined spectrophotometrically. On the other hand, the development of atherosclerotic lesions was confirmed by eosin/hematoxylin staining and electron microscopy. At the end of the experiment, total cholesterol, triglycerides, cholesterol-LDL, and cholesterol-HDL levels were significantly increased. Also, a high index of biomolecules damage, a disruption of both enzymatic and nonenzymatic defenses, and a reduction of nitric oxide were observed. Our data demonstrated that Lipofundin 20% induces hyperlipidemia, which promotes an oxidative stress state. Due to the importance of these phenomena as risk factors for atherogenesis, we suggest that Lipofundin induces atherosclerosis mainly through these mechanisms.