Abstract
We conducted experiments to elucidate the mechanism by which alpha-tocopherol (alpha-toc) concentration in the liver remarkably increases in rats treated with polychlorinated biphenyls (PCB) when excess amounts of DL-alpha-tocopheryl-acetate (alpha-toc-ac) were given. First, diets containing 5 and 50 mg of alpha-toc-ac per 100 g were respectively added with 0.05% of PCB and given to rats for 10 days, and alpha-toc distributions in tissues were determined. Next, the disappearance of alpha-toc from a ligated intestine of vitamin E (E)-deficient rats was then studied. There were no significant differences between the control and the PCB groups in alpha-toc concentrations in the liver and other tissues except a few tissues when a lower level of alpha-toc-ac (5 mg) was given. Conversely, when a higher level of alpha-toc-ac (50 mg) was given, alpha-toc concentration in the liver of the PCB group significantly increased compared to that of the control group. This agrees with the result previously reported, showing a remarkable reproducibility. In addition, alpha-toc concentrations in tissues other than the liver were also significantly higher in the PCB group than in the control group. Transmigration of alpha-toc to the liver from other tissues was therefore excluded. The alpha-toc absorption test using the ligated intestine of E-deficient rats revealed that alpha-toc disappears from the intestine at a higher rate in the presence of PCB compared to the untreated control group. This may indicate that alpha-toc absorption by passive diffusion is accelerated in the coexistence of PCB.
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