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Mangiferin: A xanthone attenuates mercury chloride induced cytotoxicity and genotoxicity in HepG2 cells
Author(s) -
Kaivalya Mudholkar,
Rao B. Nageshwar,
Satish Rao B. S.
Publication year - 2011
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.20366
Subject(s) - mangiferin , genotoxicity , chemistry , dna damage , micronucleus test , reactive oxygen species , oxidative stress , comet assay , xanthone , antioxidant , biochemistry , pharmacology , microbiology and biotechnology , dna , toxicity , stereochemistry , chromatography , biology , organic chemistry
Abstract Mangiferin (MGN), a dietary C‐glucosylxanthone present in Mangifera indica , is known to possess a spectrum of beneficial pharmacological properties. This study demonstrates antigenotoxic potential of MGN against mercuric chloride (HgCl 2 ) induced genotoxicity in HepG2 cell line. Treatment of HepG2 cells with various concentrations of HgCl 2 for 3 h caused a dose‐dependent increase in micronuclei frequency and elevation in DNA strand breaks (olive tail moment and tail DNA). Pretreatment with MGN significantly ( p < 0.01) inhibited HgCl 2 ‐induced (20 µM for 30 h) DNA damage. An optimal antigenotoxic effect of MGN, both in micronuclei and comet assay, was observed at a concentration of 50 µM. Furthermore, HepG2 cells treated with various concentrations of HgCl 2 resulted in a dose‐dependent increase in the dichlorofluorescein fluorescence, indicating an increase in the generation of reactive oxygen species (ROS). However, MGN by itself failed to generate ROS at a concentration of 50 µM, whereas it could significantly decrease HgCl 2 ‐induced ROS. Our study clearly demonstrates that MGN pretreatment reduced the HgCl 2 ‐induced DNA damage in HepG2 cells, thus demonstrating the genoprotective potential of MGN, which is mediated mainly by the inhibition of oxidative stress. © 2011 Wiley Periodicals, Inc. J Biochem Mol Toxicol 25:108–116 2011; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.20366