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Tocopherol Moderately Induces the Expressions of Some Human Sulfotransferases, which are Activated by Oxidative
Sangita MaitiDutta1, Guangping Chen2, Smarajit Maiti3,4
1Department of Biological Sciences, Midnapore City College, Midnapore, West Bengal, India.
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.
Insights
Vitamin E moderately influences sulfotransferase (SULT) expression, with tocopherol showing more induction than tocotrienol. Oxidative stress, however, activates SULT activities and expressions in both rats and humans.
Area of Science:
- Biochemistry and Molecular Biology
- Pharmacology and Toxicology
- Nutritional Science
Background:
- Oxidative stress, from environmental factors and daily life, impairs drug-metabolizing enzyme activities, specifically sulfotransferases (SULTs).
- Vitamin E (tocopherol and tocotrienol) is widely consumed for cellular protection against oxidative stress and aging.
Purpose of the Study:
- To investigate the influence of different forms of Vitamin E (tocopherol and tocotrienol) on sulfotransferase (SULT) expression and activity.
- To examine the effects of oxidative and reductive conditions on SULT activities in relevant biological tissues.
Main Methods:
- Human HepG2 cells were treated with varying concentrations of Vitamin E isomers (tocopherol and tocotrienol).
- Sulfotransferase expression was analyzed using Western blotting.
- SULT activities were measured in rat liver and human intestinal tissues under oxidant (GSSG) and reductant (GSH, DTT) conditions.
Main Results:
- Tocopherol isomers demonstrated a more significant induction of monoamine-SULT (MPST) and Dehydroepiandrosterone-SULT (DHEAST) compared to tocotrienol isomers.
- Vitamin E moderately induced the nuclear factor constitutive androstane receptor (CAR).
- Oxidative stress was found to activate both rat and human SULT activities and expressions.
Conclusions:
- Vitamin E exhibits a moderate influence on SULT expression, with tocopherol being a more potent inducer than tocotrienol.
- The long-term effects of tocopherol consumption on SULT induction warrant further consideration.
- Oxidative stress plays a role in activating SULTs, necessitating additional research into these mechanisms.
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