Carcinogenesis, Teratogenesis & Mutagenesis ›› 2010, Vol. 22 ›› Issue (3): 186-190.doi: 10.3969/j.issn.1004-616x.2010.03.007

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Vitamin E succinate induced apoptosis of SGC-7901 cells via reactive oxygen species

JIA Li1;WANG Yan-jun2;ZHANG Xu-guang1;HUANG Xiao-li1;WU Kun1   

  1. 1.Environmental Hygiene Department, Public Health Institute of Harbin Medical University, Harbin 150081; 2. Center for Disease Prevention and Control of Heilongjiang Province, Harbin 150030,Heilongjiang, China
  • Received:2009-12-15 Revised:2010-03-14 Online:2010-05-30 Published:2010-05-30
  • Contact: WU Kun

Abstract: OBJECTIVE: To study the apoptosis effect of SGC-7901 cells induced by Vitamin E succinate(VES), and explore the involvement and mechanisms of oxidative damage. METHODS: After treatment by 0, 5, 10, 20 μg/ml VES for 24 h, methods of flow cytometry, confocal laser scanning microscopy and western blot were used to measure the mitochondrial oxidative damage and apoptosis induced by VES of SGC-7901 cells. The corresponding detection kits were used to detect the reactive oxygen species and Ca2+ content. At the same time, SGC-7901 cells were treated with 1 mmol/L of mannitol for 2 h, and then 20 μg/ml VES for 24 h, and the above detection methods were used. RESULTS: With the increasing concentration of VES, apoptosis showed an increasing trend. Compared with the negative control group, ΔΨm of cells in 10, 20 μg/ml VES groups were significantly decreased, while the active oxygen content and the level of Ca2+ significantly was increased. 1 mmol/L of mannitol could impact the cells of oxygen and Ca2+ contents significantly, while significantly reduce mitochondrial oxidative damage and apoptosis caused by VES. CONCLUSION: VES could significantly increase SGC-7901 apoptosis, and with increasing doses of VES, the apoptosis rate was higher. Oxidative damage caused by raised active oxygen and Ca2+ content increasing and ΔΨm depletion in cells may be one of the mechanisms of apoptosis induced by VES.

Key words: Vitamin E succinate, active oxygens, Ca2+, oxidative damage

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