Measurement of pharmacokinetic parameters is performed by taking blood and urine samples . If your mouse strain has a tumor modification would be good to know if any liver enzyme affects especially CYP450 that are metabolizing vitamins.

Is my opinion- 

Please see the section titled "Interpatient Pharmacokinetic Variability" and its associated table: http://www.ncbi.nlm.nih.gov/books/NBK12815/

I concur with the previous answer, and I would add that changes in adipose distribution could also potentially have large effects on ADME of a fat-soluble vitamin. 

Dear Wong,

I am agreed with the previous answers. Pharmacokinetic results may be different in the healthy animals (or healthy human volunteers) in comparison of the tumour models. Because these disease states always effect on the ADME of drugs (may change the absorption, distribution, metabolism and elimination of drugs from the body).

If you are using the same strain of mice for tumor bearing vs. healthy controls - any observed PK/PD difference in a genetically homogenous murine strain, with proper balancing of sex of the animals (there can be sex differences in PK/PD) between the groups is most likely due to tumor associated stress and growth on distribution, metabolism and elimination. Vitamin E has a long half life and is lipophilic, so I would estimate that there is not going to be much difference unless there is a lot of oxidative stress in the tumor bearing mice compared to controls. 

I would like to fully share my colleague's views, especially Frederick Hausheer's colleagues, about measuring pharmacokinetic parameters, especially the role of the liver and the first passage and the role of Citohrom P-450 in metabolizing vitamin E in it!

What we can do with people in clinical trials may also be to experiment with liver transaminases (ALT, SGPT, GT etc) and to see in what state function (cirrhosis, hepatitis, fatty degeneration, steatosis, etc.) is a liver and can affect significantly To the expected results!