Research Article Effects of Dietary Cholesterol and Its Oxidation Products on Pathological Lesions and Cholesterol and Lipid Oxidation in the Rabbit Liver Sun Jin Hur, 1 Ki Chang Nam, 2 Byungrok Min, 3 Min Du, 4 Kwon Il Seo, 5 and Dong Uk Ahn 2,6 1 Department of Animal Science and Technology, Chung-Ang University, 4726 Seodong-daero, Daedeok-myeon, Anseong-si, Gyeonggi-do 456-756, Republic of Korea 2 Department of Animal Science and Technology, Sunchon National University, Suncheon 540-742, Republic of Korea 3 Food Science and Technology Program, Department of Agriculture, Food, and Resource Sciences, University of Maryland Eastern Shore, Princess Anne, MD 21853, USA 4 Department of Animal Science, Washington State University, Pullman, WA 99164-6310, USA 5 Department of Food and Nutrition, Sunchon National University, Suncheon 540-742, Republic of Korea 6 Department of Animal Science, College of Agriculture, Iowa State University, Ames, IA 50011, USA Correspondence should be addressed to Dong Uk Ahn; duahn@iastate.edu Received 22 November 2013; Accepted 19 December 2013; Published 20 February 2014 Academic Editor: Kusum Kharbanda Copyright © 2014 Sun Jin Hur et al. Tis 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. Tis study was conducted to determine the efects of dietary cholesterol (CHO) and cholesterol oxidation products (COPs) on the induction of pathological lesions in rabbit liver tissues. Liver lesions were induced only when the levels of CHO and COPs in the diet were very high. Te amount of CHO measured in the liver increased when dietary CHO was increased; by comparison, dietary COPs afected liver CHO amounts to a lesser extent. Te TBARS (thiobarbituric acid reactive substances) value measured for the liver samples also increased when dietary CHO and COP levels were elevated, and the TBARS value was more strongly afected by the amount of COPs in the diet than by the amount of CHO. At 6 and 12 weeks, COP levels were the highest in the group that received 1.2 g CHO + 0.8 g COPs, followed by the 0.5 g CHO + 0.5 g COPs and 1.6 g CHO + 0.4 g COPs groups; the control (0 g) group showed the lowest COP levels among all groups. In this study, we found that not only dietary CHO but also COPs were involved in hypercholesterolemia induced liver lesions when the amount of CHO and COPs was high. 1. Introduction Cholesterol (CHO) is a crucial component of the human body, but a high level of CHO is considered a major risk factor for the development of atherosclerosis and coronary heart disease (CHD) [1]. Moreover, the intake of cholesterol oxida- tion products (COPs) also typically leads to the development of atherosclerosis and CHD [2]. CHO is widely distributed in living organisms and is localized mainly in cell membranes in its nonesterifed form [3] and in the blood as a component of lipoproteins mainly in its esterifed form [4], and CHO plays a role in numerous physiological and pathological processes. CHO may be derived either from the diet or by means of endogenous synthesis, which occurs primarily in the liver [4]. Te liver is also the major site where CHO is removed by being directly secreted into the bile or by being broken down into bile acids; moreover, the liver plays a key role in maintaining whole body CHO homeostasis by controlling the uptake of extracellular CHO, CHO synthesis, and CHO storage [5]. An elevated level of plasma CHO is typically a risk factor for atherosclerosis, and several COPs are cytotoxic, atherogenic, mutagenic, or carcinogenic; furthermore, COPs injure endothelial cells, leading to atherosclerosis [1]. Alter- ations in hepatic CHO homeostasis caused by dietary or drug interventions potently infuence CHO balance and plasma low density lipoprotein (LDL) CHO levels in the body [6]. Tus, dietary CHO and COPs critically afect health because LDL CHO levels are positively correlated with the risk of Hindawi Publishing Corporation BioMed Research International Volume 2014, Article ID 598612, 7 pages http://dx.doi.org/10.1155/2014/598612