We previously reported that heat pretreatment of corn fiber (150 degrees C, 1 h) caused a tenfold increase in the levels of extractable gamma-tocopherol. The current study was a reinvestigation of the previous effect, using improved methods (HPLC with fluorescence detection, diode-array UV detection, and mass spectrometry) for tocol analysis. Heat pretreatment did not cause an increase in the levels of any of the tocopherols or tocotrienols in corn fiber oil, but lowered the levels of three of the tocols and had no effect on the levels of the other two tocols. Heat pretreatment of corn germ had a similar effect. UV and mass spectra indicated that the peak that we had identified as gamma-tocopherol in our previous report was probably a mixture of oxidation products of triacylglycerols. Thus, heat treatment of corn germ or other corn-oil containing fractions at high temperatures leads to decreases in gamma-tocopherol, gamma-tocotrienol, and delta-tocotrienol and to the production of triacylglycerol oxidation products.
We evaluated the antitumor activity of tocotrienol (T3) on human hepatoma Hep3B cells. At first, we examined the effect of T3 on the proliferation of human hepatoma Hep3B cells and found that gamma-T3 inhibited cell proliferation at lower concentrations and shorter treatment times than alpha-T3. Then, we examined the effect of gamma-T3 apoptosis induction and found that gamma-T3 induced poly (ADP-ribose) polymerase (PARP) cleavage and stimulated a rise in caspase-3 activity. In addition, gamma-T3 stimulated a rise in caspase-8 and caspase-9 activities. We also found that gamma-T3-induced apoptotic cell death was accompanied by up-regulation of Bax and a rise in the fragments of Bid and caspase-8. These data indicate that gamma-T3 induced apoptosis in Hep3B cells and that caspase-8 and caspase-9 were involved in apoptosis induction. Moreover, these results suggest that Bax and Bid regulated apoptosis induction by gamma-T3.