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Your Environment. Your Health.

Final Progress Reports: University of Kentucky: Mechanisms of Hepatic Tumor Promotion by PCBs

Superfund Research Program

Mechanisms of Hepatic Tumor Promotion by PCBs

Project Leader: Howard P. Glauert
Grant Number: P42ES007380
Funding Period: 1997 - 2005

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Final Progress Reports

Year:   2004  1999 

The main goal of this project is to determine the mechanisms by which PCBs exert their promoting activity in liver carcinogenesis, i.e., ways in which they cause the progression of pre-cancerous lesions from a biochemical lesion (DNA damage) to a visible tumor.  The investigators have hypothesized that the results from the induction of oxidative stress, and therefore that increasing antioxidants in the diet could inhibit tumor promotion by PCBs.  In the past year, the team has carried out two dietary studies.  In the first, they examined if dietary selenium could inhibit the promoting activities of PCB-77 and PCB-153.  Although the highest level of selenium decreased the average size of the preneoplastic lesions induced, the number of lesions per liver was increased.  In the second study, they examined whether phytochemicals could inhibit the promoting activity of PCB-77.  β-Carotene was the most effective, with lycopene and curcumin having a lesser effect, and ellagic acid, N-acetyl cysteine, resveratrol, EGCG, and coenzyme Q-10 being ineffective.  Therefore, certain antioxidants can inhibit the promoting activities of PCBs whereas others cannot.  Another goal is to determine the role of non-hepatocytes such as Kupffer cells in the promoting activity of PCBs, using both in vivo and in vitro models.  Using the in vitro model, the investigators have observed that PCB-153 treatment increased NF-κB activation and tumor necrosis factor-α (TNF-α) secretion by Kupffer cells isolated by centrifugal elutriation. 

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