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Journal of Environmental Pathology, Toxicology and Oncology
IF: 1.241 5-Year IF: 1.349 SJR: 0.356 SNIP: 0.613 CiteScore™: 1.61

ISSN Print: 0731-8898
ISSN Online: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.v30.i4.10
pages 273-282

Role of Oil Vehicle on Hepatic Cell Proliferation in PCB-Treated Rats

Rodica Petruta Bunaciu
Graduate Center for Nutritional Sciences, University of Kentucky, Lexington, Kentucky
Job C. Tharappel
Graduate Center for Nutritional Sciences, University of Kentucky, Lexington, Kentucky
Hans-Joachim Lehmler
Department of Occupational and Environmental Health, University of Iowa, Iowa City, Iowa
Eun Y. Lee
Departments of Pathology and Laboratory Medicine, University of Kentucky, Lexington, Kentucky
Larry W. Robertson
Department of Occupational and Environmental Health, University of Iowa, Iowa City, Iowa
Geza G. Bruckner
Graduate Center for Nutritional Sciences, University of Kentucky, Lexington, Kentucky; Departments of Clinical Sciences , University of Kentucky, Lexington, Kentucky
Brett T. Spear
Departments of Microbiology, Immunology, and Molecular Genetics, University of Kentucky, Lexington, Kentucky; and Markey Cancer Center, University of Kentucky, Lexington, Kentucky
Howard P. Glauert
Graduate Center for Nutritional Sciences, University of Kentucky, Lexington, Kentucky;Markey Cancer Center, University of Kentucky, Lexington, Kentucky;

ABSTRACT

We report the role of dietary glycine and the type of oil used as a vehicle in the hepatotoxicity of control rats and rats treated with 2,2’,4,4’,5,5’-hexachlorobiphenyl (PCB-153). In our first experiment, glycine or valine (as control) was fed in an unrefined diet at 5% for the entire study duration (5 days) to inhibit Kupffer cell activity. PCB-153 (100 or 300 μmol/kg) dissolved in medium chain triglyceride (MCT) oil, was injected intraperitoneally 2 days before euthanasia; the peroxisome proliferator Wy-14,643 was included as a positive control. MCT oil decreased cell proliferation by approximately 50%. PCB-153 slightly increased hepatic cell proliferation, but dietary glycine did not reduce cell proliferation. Because of the inhibition of cell proliferation in rats receiving MCT oil compared with rats receiving no injection, we hypothesized that MCT oil may have been inhibiting the hepatocyte proliferation in PCB-153−treated rats. We therefore performed another experiment using 3 types of oil as a vehicle for PCB-153: MCT oil, corn oil, and olive oil. Rats were injected with PCB-153 (300 μmol/kg) or one of the vehicles, again 2 days before euthanasia. MCT oil again decreased the hepatocyte proliferation by approximately 50%. In rats receiving PCB-153, hepatocyte proliferation was slightly higher than their respective vehicle controls for corn oil and olive oil but not for MCT oil. These studies show that the oil vehicle is important in cell proliferation after PCB exposure, with MCT oil appearing to be protective.


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