Abstract:
Oxidative stress is generated in biological system by several endogenous/exogenous factors like environmental-pollution/
toxicity/diseases and by daily-life-stress. We previously showed that oxidative-stress impaired the activities/expressions of
phase-II drug-metabolizing enzyme, sulfotransferases (SULTs). The SULT catalyzes sulfation of endogenous/exogenous
compounds. Vitamin E is globally consumed by a large number of individuals for the cellular protection from oxidative
stress and aging. Here, vitamin E (tocopherol; α/γ and tocotrienol; α/γ; 0, 1, 10, or 100 μM) was tested in human carcinoma
cell line, HepG2 for their influences on SULTs expression/(western blotting). The effects of oxidant (glutathione-oxidized/
GSSG) or reductant (glutathione-reduced/GSH, Dithiothreitol/DTT) on SULT activities were studied in rat-liver/human
intestinal tissues. Results suggest, tocopherol is more inductive to monoamine-SULT (MPST) and Dehydroepiandrosterone-
SULT (DHEAST) compared to that of tocotrienol (inconsistent change in PPST, phenol sulfotransferase/MPST/EST,
estrogen sulfotransferase). The nuclear-factor constitutive androstane receptor (CAR) was found to be induced moderately.
This study overall describes that vitamin E moderately influences SULTs expression. The induction ability of tocopherol
should be judged taking into account its long-term consummation. Oxidative stress activates rat and human SULTs activities
and expressions. Further studies are necessary in this regard.
