%0 Journal Article
%T Lipofundin-Induced Hyperlipidemia Promotes Oxidative Stress and Atherosclerotic Lesions in New Zealand White Rabbits
%A Livan Delgado Roche
%A Emilio Acosta Medina
%A ¨¢ngela Fraga P¨¦rez
%A Mar¨ªa A. B¨¦cquer Viart
%A Yosdel Soto L¨®pez
%A Viviana Falc¨®n Cama
%A Ana M. V¨¢zquez L¨®pez
%A Gregorio Mart¨ªnez-S¨¢nchez
%A Eduardo Fern¨¢ndez-S¨¢nchez
%J International Journal of Vascular Medicine
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/898769
%X 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. 1. Introduction Atherosclerosis is a chronic vascular disease and a leading cause of death in the western world. It is well established that hyperlipidemia and oxidative stress (OS) are major contributors to atherogenic development [1]. The retention of low-density lipoproteins (LDL) in the arterial wall [2] and their oxidation by reactive oxygen species (ROS) initiates a complex series of biochemical and inflammatory reactions [3, 4]. Oxidized LDL (ox-LDL) are internalized by macrophages through the scavenger receptors, leading to foam cell formation [5]. Furthermore, oxidized cholesterol products present in blood and in arterial plaques increase cholesterol biosynthesis, affect plasma membrane structure, cell proliferation, and cell death, and promotes atherosclerosis development [6]. The rabbit is one of the most widely used animal models in atherosclerosis research. One strategy to induce atherosclerotic lesions in these animals is through an intravenous administration of Lipofundin 20%, a lipid-rich emulsion used in parenteral nutrition, which produces aortic lesions, characterized by subendothelial lipid accumulation, intimal thickening, and a distortion of vascular tissue architecture [7, 8]. The impact of Lipofundin 20% administration on lipid levels and redox environment in New Zealand white (NZW) rabbits had not been studied. In the present work, we demonstrated that Lipofundin 20% induces a hyperlipemic state and a systemic/aortic oxidative stress, which can lead to atherosclerotic
%U http://www.hindawi.com/journals/ijvm/2012/898769/