Carcinogenesis, Teratogenesis & Mutagenesis ›› 2009, Vol. 21 ›› Issue (5): 372-376.doi: 10.3969/j.issn.1004-616x.2009.05.010

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Oxidative Damage of Mitochondria by Olaquindox in HepG2 Cells

ZOU Jia-jie; ZHANG Ting; TANG Shu-sheng; CHEN Qian; JIN Xi;CHEN Kai-pao; XIAO Xi-long   

  1. Department of Pharmacology and Toxicology, College of Veterinary Medicine, China Agriculture University, Beijing 100193, China
  • Received:2009-01-05 Revised:2009-04-23 Online:2009-09-30 Published:2009-09-30
  • Contact: XIAO Xi-long

Abstract: BACKGROUND AND AIM: To investigate oxidative damage of mitochondria induced by olaquindox in human hepatoma G2 (HepG2) cells. MATERIALS AND METHODS: HepG2 cells were treated with 0,200,400 and 800 μg/ml olaquindox for 24 h. The value of IC50 of olaquindox in HepG2 cells was determined by MTT assay. The levels of reactive oxygen species (ROS) were detected by 2, 7-dichlorodihydrofluorescein diacetate (DCFDA) and Dihydroethidium (DHE). The level of mitochondrial membrane potential(△Ψm) and calcium concentration were measured by Rhodamine123(Rh-123) and Fluo-3AM, respectively. Finally, the damage ratio of mtDNA and nDNA was assessed by quantitative PCR. RESULTS: MTT assay revealed that the HepG2 cells viabilities were significantly inhibited by olaquindox in dose- and time- dependent manners. Olaquindox induced increased levels of ROS and calcium in HepG2 cells, and reduced the level of △Ψm . Quantitative PCR assay showed that olaquindox led to a dose-dependent decrease in the amplification of both mtDNA and nDNA. These data also suggested that the olaquindox-induced damage to mtDNA was more extensive than its damage to nDNA. CONCLUSION: Olaquindox could cause oxidative damage of mitochondria in HepG2 cells.

Key words: olaquindox, mitochondria, reactive oxygen species, mitochondrial membrane potential, calcium

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