Inhibition of Sudan I genotoxicity in human liver-derived HepG2 cells by the antioxidant hydroxytyrosol.

Abstract

The chemoprotective effect of hydroxytyrosol (HT) against Sudan I-induced genotoxicity was investigated in a human hepatoma cell line, HepG2. The comet assay and micronucleus (MN) assay were used to monitor genotoxicity. Intracellular reactive oxygen species (ROS) formation was measured using a fluorescent probe, 2,7-dichlorofluorescein diacetate (DCFH-DA). The levels of oxidative DNA damage and lipid peroxidation were estimated by immunocytochemistry analysis of 8-hydroxydeoxyguanosine (8-OHdG) and by measuring levels of thiobarbituric acid-reactive substances (TBARS), respectively. Intracellular glutathione (GSH) level was estimated by fluorometric methods. The results showed that HT significantly reduced the genotoxicity caused by Sudan I. Furthermore, HT ameliorated lipid pexidation as demonstrated by a reduction in TBARS formation and attenuated GSH depletion in a concentration-dependent manner. It was also found that HT reduced intracellular ROS formation and 8-OHdG level caused by Sudan I. These results strongly suggest that HT has significant protective ability against Sudan I-induced genotoxicity.

• Authors: Xiaomei Zhang, Liping Jiang, Chengyan Geng, Cunli Hu, Hiroyuki Yoshimura, Laifu Zhong
• Journal: Free radical research (Free Radic Res) Vol. 42 Issue 2 Pg. 189-95 (Feb 2008) ISSN: 1071-5762 [Print] England
• PMID: 18297612 (Publication Type: Journal Article)

Chemical References

• Antioxidants
• Mutagens
• Naphthols
• Reactive Oxygen Species
• 3,4-dihydroxyphenylethanol
• 1-phenylazo-2-naphthol
• 8-Hydroxy-2'-Deoxyguanosine
• Deoxyguanosine
• Glutathione
• Phenylethyl Alcohol

Topics

• 8-Hydroxy-2'-Deoxyguanosine
• Antioxidants (pharmacology)
• Cell Line, Tumor
• DNA Damage (drug effects)
• Deoxyguanosine (analogs & derivatives, metabolism)
• Glutathione (metabolism)
• Humans
• Lipid Peroxidation (drug effects)
• Micronucleus Tests
• Mutagens (toxicity)
• Naphthols (antagonists & inhibitors, toxicity)
• Phenylethyl Alcohol (analogs & derivatives, pharmacology)
• Reactive Oxygen Species (metabolism)