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Inhibitory effects of various beverages on human recombinant sulfotransferase isoforms SULT1A1 and SULT1A3
Author(s) -
Nishimuta Haruka,
Ohtani Hisakazu,
Tsujimoto Masayuki,
Ogura Kenichiro,
Hiratsuka Akira,
Sawada Yasufumi
Publication year - 2007
Publication title -
biopharmaceutics and drug disposition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.419
H-Index - 58
eISSN - 1099-081X
pISSN - 0142-2782
DOI - 10.1002/bdd.579
Subject(s) - chemistry , bioavailability , naringin , quercetin , theaflavin , pharmacology , biochemistry , food science , traditional medicine , polyphenol , biology , chromatography , medicine , antioxidant
Sulfotransferase (SULT) 1A1 and SULT1A3 play important roles in the presystemic inactivation of β 2 agonists in the liver and intestine, respectively. The study aimed to investigate the inhibitory effects of grapefruit juice, orange juice, green tea, black tea and oolong tea and their constituents on the activities of SULT1A1 and SULT1A3. The activities of both SULT1A1 and SULT1A3 were significantly inhibited by all the beverages investigated at a concentration of 10%. The beverage constituents were tested in concentration ranges considered to be physiologically relevant. The grapefruit constituent, quercetin, completely inhibited SULT1A1, while quercetin and naringin both partially inhibited SULT1A3. The orange constituents, tangeretin and nobiletin, also completely inhibited SULT1A1. The tea constituents, (−)‐epicatechin gallate and (−)‐epigallocatechin gallate, both almost completely inhibited SULT1A1 and SULT1A3. Moreover, the theaflavin and thearubigin fractions of black tea both completely inhibited SULT1A1 and strongly inhibited SULT1A3. The inhibitory action of green tea on SULT1A3 was competitive, while that of black tea and oolong tea was mixed competitive/non‐competitive. Mechanism‐based inhibition was not observed with any beverage. In conclusion, various beverages, especially teas, inhibit the function of SULT1A3, and therefore may have the potential to increase the bioavailability of orally administered substrates of SULT1A3, such as β 2 agonists. Copyright © 2007 John Wiley & Sons, Ltd.