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Mangiferin: A xanthone attenuates mercury chloride induced cytotoxicity and genotoxicity in HepG2 cells

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 (HgCl2) induced genotoxicity in HepG2 cell line. Treatment of HepG2 ce...

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Published in:Journal of biochemical and molecular toxicology 2011-03, Vol.25 (2), p.108-116
Main Authors: Kaivalya, Mudholkar, Rao, B. Nageshwar, Satish Rao, B. S.
Format: Article
Language:English
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Summary: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 (HgCl2) induced genotoxicity in HepG2 cell line. Treatment of HepG2 cells with various concentrations of HgCl2 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 HgCl2‐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 HgCl2 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 HgCl2‐induced ROS. Our study clearly demonstrates that MGN pretreatment reduced the HgCl2‐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
ISSN:1095-6670
1099-0461
1099-0461
DOI:10.1002/jbt.20366