Growth inhibition and antioxidative status induced by selenium-enriched broccoli extract and selenocompounds in DNA mismatch repair-deficient human colon cancer cells

• Published in: Food chemistry 2013-08, Vol.139 (1-4), p.267-273
• Main Authors: Tsai, Cheng-Fang, Ou, Bor-Rung, Liang, Yu-Chuan, Yeh, Jan-Ying
• Format: Article
• Language: English
• Subjects: Antioxidants - pharmacology; Biological and medical sciences; Brassica - chemistry; Broccoli extract; Cell Proliferation - drug effects; Cellular glutathione peroxidase (cGPX); Colonic Neoplasms - drug therapy; Colonic Neoplasms - genetics; Colonic Neoplasms - metabolism; Colonic Neoplasms - physiopathology; DNA Mismatch Repair - drug effects; Food industries; Fruit and vegetable industries; Fundamental and applied biological sciences. Psychology; HCT116 Cells; Human colon cancer cells; Humans; Hydrogen peroxide (H2O2); Hydrogen Peroxide - metabolism; Plant Extracts - pharmacology; Selenium; Selenium - pharmacology; Selenium Compounds - pharmacology
• ISSN: 0308-8146; 1873-7072
• DOI: 10.1016/j.foodchem.2013.02.001

► The cytotoxicity of selenite in two HCT116 cells was related to H2O2 production. ► The difference in cytotoxicity of selenite between two HCT116 cells may be due to chromosome 3. ► H-SeB reduced but selenite increased H2O2 content in HCT116+ch3. ► Regardless of Se content, HCT116 cytotoxicity of either SeB was H2O2-independent. ► HCT116+ch3 cytotoxicity of either SeB was H2O2-dependent, regardless of Se content. The effects of enzymatic-digested Se-enriched broccoli extracts (SeB) and selenocompounds on growth and antioxidative status in human colon cancer cells was investigated in this study. HCT116 and HCT116+Chr.3 cells were treated with selenocompounds (sodium selenite, sodium selenate, Se-Met, MeSeCys) or SeB [high-Se (H-SeB) or low-Se (L-SeB)]. The cytotoxicity induced by selenocompounds in HCT116 cells was not associated with cellular H2O2 level, while the differential cytotoxicity observed by sodium selenite between HCT116 and HCT116+Chr.3 cell lines was related to cellular H2O2 production with the change in antioxidative enzyme activity, and the restoration of chromosome 3. H-SeB was found to reduce the cellular H2O2 content in HCT116+Chr.3 cells. The results in this study indicate that regardless of Se content, the cytotoxicity in HCT116 cells of both SeB forms appeared to be H2O2-independent, whereas the cytotoxicity in HCT116+Chr.3 of either SeB form appeared to be H2O2-dependent with an increase in antioxidative ability for H-SeB.