Abstract | AIMS: MAIN METHODS: Antioxidation in vitro was determined from elimination of the DPPH radical, ferric reducing- antioxidant power (FRAP), O2(-), and peroxyl radical scavenging activity. Intracellular O2(-), H2O2 and GSH levels were determined by DHE, DCFH-DA, and CMF-DA assay, respectively. Cell viability was detected by neutral red assay. Cell cycle proportion and mode of apoptotic HCT116 cells death was analyzed by flow cytometry. Apoptosis in sesamol-treated HCT116 cells was confirmed by morphological changes in the nuclei using DAPI staining and changes in mitochondrial membrane potential using the DiOC6(3) assay. KEY FINDINGS:
Sesamol at both low (0.05 and 0.25mM) and high (0.5, 2, 5, and 10mM) concentrations concurrently reduced FRAP reagent and scavenged DPPH, and O2(-). Sesamol at low concentrations scavenged ROO, but ROO-scavenging was decreased at higher concentrations. Sesamol suppressed cell viability via disruption of cell cycle progression at high concentrations (0.5, 1, 2, and 5mM), thereby causing S-phase arrest and inducing apoptosis-through the production of intracellular O2(-), mitochondrial dysfunction, and DNA fragmentation. SIGNIFICANCE:
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Authors | Munthipha Khamphio, Sahapat Barusrux, Natthida Weerapreeyakul |
Journal | Life sciences
(Life Sci)
Vol. 158
Pg. 46-56
(Aug 01 2016)
ISSN: 1879-0631 [Electronic] Netherlands |
PMID | 27328416
(Publication Type: Journal Article)
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Copyright | Copyright © 2016 Elsevier Inc. All rights reserved. |
Chemical References |
- Benzodioxoles
- Phenols
- Reactive Oxygen Species
- sesamol
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Topics |
- Apoptosis
(drug effects)
- Benzodioxoles
(pharmacology)
- Cell Cycle
(drug effects)
- Colonic Neoplasms
(pathology)
- HCT116 Cells
- Humans
- Mitochondria
(drug effects)
- Phenols
(pharmacology)
- Reactive Oxygen Species
(pharmacology)
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