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J.Health Sci., 55(6), 901-909, 2009
Persistent Exposure to 2,3',4,4',5-Pentachlorobiphenyl (PCB118) Induces Hyperalphacholesterolemia in Rats
Dae-Yong Han,a Hyeon-Soo Park,a
Kwang-Il Park,a Sang-Rim Kang,a
Jae-Hyeon Cho,a Won-Sup Lee,b
Eun-Ju Kim,c Eun-Hee Kim,d
and Gon-Sup Kim*, a
aResearch Institute of Life Science and College of Veterinary Medicine, Gyeongsang National University, 900 Gajwadong, Jinju, Gyeongnam 660-701, Korea,
bDepartment of Internal Medicine, Gyeongnam Regional Cancer Center, Institute of Health Sciences, Gyeongsang National University, 92 Chiramdong, Jinju, Gyeongnam 660-702, Korea,
cDepartment of Information and Communication Engineering, Tongmyong University, 179 Shinsunro, Nam-gu, Pusan 608-711, Korea and
dDepartment of Physical Therapy, International University of Korea, 270 Sangmun-lee, Munsan-eup, Jinju 660-759, Korea
Polychlorinated biphenyls (PCBs) are synthetic organic compounds with two phenyl groups well known environmental pollutants. This study examined the effect of persistent exposure to 2,3',4,4',5-pentachlorobiphenyl (PCB118) on serum cholesterol levels in male rats. Male Sprague Dawley rats were administered weekly intraperitoneal injections of either PCB118 (20 mg/kg) dissolved in corn oil or corn oil alone. One week after 2 and 5 administrations, the rats were sacrificed by a pentobarbital injection, and the effect of PCB118 on the serum levels of total cholesterol, high density lipoprotein-cholesterol (HDL-cholesterol), and low density lipoprotein-cholesterol (LDL-cholesterol) was investigated. The protein expression level of apolipoprotein A-I (apo A-I) and 3-hydroxy-3-methylgulutaryl coenzyme A (HMG-CoA) reductase was also examined. In this study, the administration of PCB118 induced hyperalphacholesterolemia in rats. In addition, the protein expression level of HMG-CoA reductase and apo A-I was higher in the PCB118-treated rats than in the control. These results suggest that the hyperalphacholesterolemia induced by PCB118 in male rats may be associated with an increase in HMG-CoA reductase and apo A-I expression.
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