Mangiferin glucuronidation: important hepatic modulation of antioxidant activity.

Autor: van der Merwe JD; Department of Food Science, Stellenbosch University, Private Bag X1, Matieland, Stellenbosch 7602, South Africa., Joubert E, Manley M, de Beer D, Malherbe CJ, Gelderblom WC
Jazyk: angličtina
Zdroj: Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association [Food Chem Toxicol] 2012 Mar; Vol. 50 (3-4), pp. 808-15. Date of Electronic Publication: 2011 Nov 25.
DOI: 10.1016/j.fct.2011.11.018
Abstrakt: Mangiferin displays an extensive spectrum of pharmacological properties, including antioxidant activity. Its phase II metabolism in the presence of Aroclor 1254-induced and un-induced microsomal and cytosolic fractions from rat liver and the antioxidant potency of the glucuronidated conjugates were investigated. Mangiferin was not a substrate for the cytosolic sulphotransferases. Glucuronidation led to the formation of two monoglucuronidated metabolites of mangiferin and a monoglucuronidated metabolite of homomangiferin (a minor constituent of the mangiferin standard). Deconjugation utilising glucuronidase resulted in the disappearance of the metabolites, with the concomitant formation of the two parent compounds. Considering steric hinderance caused by the C-2 glucosyl moiety and the relative acidity of the xanthone OH groups, the 6-OH of mangiferin and, to a lesser degree the 7-OH, are likely to be the primary glucuronidation targets. The ferric iron reducing ability of the glucuronidated reaction mixture was reduced, while the free radical scavenging abilities of mangiferin, utilising on-line post-column HPLC-DAD-DPPH· and HPLC-DAD-ABTS·+ assays, were eliminated, providing further evidence that the catechol arrangement at C-6 and C-7 was the preferred site of conjugation. This paper provides the first evidence that the glucuronidated metabolites of mangiferin resulted in a loss in free radical scavenging and ferric iron reducing ability.
(Copyright © 2011 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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