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Sudan I induces genotoxic effects and oxidative DNA damage in HepG2 cells.

Abstract
Sudan I, a synthetic lipid soluble azo pigment, is widely used in various industrial fields. However, Sudan I has not been approved at any level of food production, since there are many inconclusive reports relating to its genotoxicity and carcinogenicity in humans. The aim of this study was to assess the genotoxic effects of Sudan I and to identify and clarify the reaction mechanisms by use of human hepatoma HepG2 cells. To study the genotoxic effects of Sudan I, the comet assay and micronucleus test (MNT) were used. In the comet assay and MNT, we found increase of DNA migration and of the micronuclei frequencies at all tested concentrations (25-100 microM) of Sudan I in a dose-dependent manner. The data suggest that Sudan I caused DNA strand breaks and chromosome breaks. To elucidate the underlying mechanism of this difference, we monitored the level of reactive oxygen species (ROS) production with the 2,7-dichlorofluorescein diacetate assay. The level of the oxidative DNA damage and lipid peroxidation was evaluated using immunoperoxidase staining for 8-hydroxydeoxyguanosine (8-OHdG) and by measuring levels of thiobarbituric acid-reactive substances (TBARS). Significantly increased levels of ROS, 8-OHdG and TBARS were observed in HepG2 cells at higher concentrations, the doses being 100, 50-100 and 50-100 microM, respectively. We conclude that Sudan I causes genotoxic effects, probably via ROS-induced oxidative DNA damage at the higher doses.
AuthorsYu An, Liping Jiang, Jun Cao, Chengyan Geng, Laifu Zhong
JournalMutation research (Mutat Res) Vol. 627 Issue 2 Pg. 164-70 (Mar 05 2007) ISSN: 0027-5107 [Print] Netherlands
PMID17188558 (Publication Type: Journal Article)
Chemical References
  • Carcinogens
  • Naphthols
  • Reactive Oxygen Species
  • 1-phenylazo-2-naphthol
Topics
  • Carcinogens (pharmacology)
  • Carcinoma, Hepatocellular (pathology)
  • Comet Assay
  • DNA Damage (drug effects)
  • DNA Fragmentation (drug effects)
  • Humans
  • Naphthols (pharmacology)
  • Oxidative Stress (drug effects)
  • Reactive Oxygen Species (metabolism)
  • Tumor Cells, Cultured

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